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J Korean Med Sci. 2025 Sep 15;40(36):e233. doi: 10.3346/jkms.2025.40.e233.

ABSTRACT

BACKGROUND: Patients undergoing extracorporeal membrane oxygenation are at a high risk of developing intracranial hemorrhage as a neurological complication. Consequently, many physicians consider a history of intracranial hemorrhage as a relative contraindication for extracorporeal membrane oxygenation and are hesitant to use it in these patients, even in cases of acute severe heart or lung failure. This study aimed to examine the clinical outcomes of extracorporeal membrane oxygenation use in patients with intracranial hemorrhage.

METHODS: We retrospectively obtained the medical records of patients diagnosed with intracranial hemorrhage who received extracorporeal membrane oxygenation owing to acute cardiopulmonary failure between January 2011 and July 2020. Data pertaining to patients' characteristics and clinical outcomes were collected. Disseminated intravascular coagulation score and extracorporeal membrane oxygenation score before and after application of extracorporeal membrane oxygenation were also examined to observe trends.

RESULTS: Eighteen patients were included. Ten had traumatic intracranial hemorrhage, and the most common indication for extracorporeal membrane oxygenation was acute respiratory distress syndrome. The 30-day survival rate was 72% (13 patients), and 61% (11 patients) survived to discharge. Two patients underwent neurosurgery due to worsening of intracranial hemorrhage. However, both were discharged without neurological deterioration.

CONCLUSION: A 72% survival rate was observed in extracorporeal membrane oxygenation patients with intracranial hemorrhage, suggesting that extracorporeal membrane oxygenation could be a viable option in patients with intracranial hemorrhage unresponsive to conventional therapy.

PMID:40955613 | PMC:PMC12437245 | DOI:10.3346/jkms.2025.40.e233

Korean J Pain. 2025 Oct 1;38(4):437-448. doi: 10.3344/kjp.25149. Epub 2025 Sep 17.

ABSTRACT

BACKGROUND: The erector spinae plane (ESP) block has gained attention as a regional anesthesia technique for pain management in vertebral surgeries. This umbrella review synthesizes data from systematic reviews (SRs) and meta-analyses to evaluate the effectiveness of the ESP block in reducing postoperative opioid consumption, pain, and postoperative nausea and vomiting (PONV) in patients undergoing vertebral surgeries.

METHODS: A search was conducted in CENTRAL, Embase, PubMed Central, and Scopus from 2016 to 2025. The authors included SRs and meta-analyses that investigated the use of the ESP block in vertebral surgeries. Primary outcomes were opioid consumption at 24 postoperative hours (measured as milligrams of morphine equivalent), pain scores at 12 and 24 hours, PONV incidence, and the need for additional analgesics. Quality was assessed using the AMSTAR 2 tool.

RESULTS: Thirteen SRs were included. The ESP block reduced opioid consumption at 24 postoperative hours (mean morphine equivalents difference, -8.70 to -18.69), although high heterogeneity was observed. Pain reduction at 12 and 24 hours was statistically significant but clinically modest, with most SRs reporting reductions of less than one point in Numeric Rating Scale or Visual Analog Scale pain scales. The ESP block also significantly reduced PONV and additional analgesic use. However, most SRs were rated as low quality due to inadequate pre-registration and justification for excluding studies.

CONCLUSIONS: The ESP block demonstrates potential as a multimodal analgesia component in vertebral surgeries, reducing opioid consumption, pain intensity, and PONV. However, high heterogeneity and low methodological quality highlight the need for further research.

PMID:40957865 | PMC:PMC12485463 | DOI:10.3344/kjp.25149

J ECT. 2025 Sep 16. doi: 10.1097/YCT.0000000000001187. Online ahead of print.

ABSTRACT

OBJECTIVES: Electroconvulsive therapy (ECT), which is applied by producing a seizure with an electrical current under general anesthesia, is an effective and reliable method in the treatment of most psychiatric diseases. Nevertheless, how the treatment affects intracranial pressure and other neuronal mechanisms is uncertain. This prospective observational study evaluated the effects of ECT on intracranial pressure by measuring the optic nerve sheath diameter (ONSD) using ultrasonography.

METHODS: Thirty-nine patients undergoing their first ECT session were included in the study, and ONSD measurements were performed on all patients at 4 time points: before and after anesthesia induction, after ECT (post-ictal), and during the recovery phase. Age, weight, height, psychiatric diagnoses, medications and comorbidities, blood pressure and heart rate values, and motor seizure durations were recorded.

RESULTS: Post-ictal ONSD (5.47 ± 0.40 mm) was significantly higher than preinduction (4.89 ± 0.33 mm), postinduction (4.90 ± 0.35 mm), and recovery (4.96 ± 0.38 mm) measurements (P < 0.001). The change in ONSD during ECT was significantly higher in patients with preexisting hypertension (P = 0.001) and correlated positively with blood pressure.

CONCLUSIONS: In patients with an indication for ECT and without an intracranial space-occupying lesion, ECT procedure may cause a transient increase in intracranial pressure (ICP). This change in ICP may be more pronounced in patients with a diagnosis of hypertension. These findings highlight the need for careful monitoring of ICP in hypertensive patients undergoing ECT.

PMID:40956101 | DOI:10.1097/YCT.0000000000001187

World J Cardiol. 2025 Aug 26;17(8):107437. doi: 10.4330/wjc.v17.i8.107437.

ABSTRACT

Mesenchymal stem cells (MSCs) possess unique properties such as immunomodulation, paracrine actions, multilineage differentiation, and self-renewal. Therefore, MSC-based cell therapy is an innovative approach to treating various degenerative illnesses, including cardiovascular diseases. However, several challenges, including low transplant survival rates, low migration to the ischemic myocardium, and poor tissue retention, restrict the application of MSCs in clinical settings. These undesirable cell therapy outcomes mainly originated due to the overproduction of reactive oxygen species (ROS) in the injured heart. MSCs' stress-coping capacity can be enhanced by preconditioning them under conditions similar to the microenvironment of wounded tissues. Hydrogen peroxide (H2O2) is a ROS that has been shown to activate protective cellular mechanisms such as survival, proliferation, migration, paracrine effects, and differentiation at sublethal doses. These processes are induced via phosphatidylinositol 3-kinase/protein kinase B, p38 mitogen-activated protein kinases, c-Jun N-terminal kinase, Janus kinase/signal transducer and activator of the transcription, Notch1, and Wnt signaling pathways. H2O2 preconditioning could lead to many clinical benefits, including ischemic injury reduction, enhanced survival of cellular transplants, and tissue regeneration. In this review, we present an overview of stem cell preconditioning methods and the biological functions activated by H2O2 preconditioning. Furthermore, this review explores the molecular mechanisms underlying the protective cellular functions stimulated under H2O2 preconditioning.

PMID:40949936 | PMC:PMC12426982 | DOI:10.4330/wjc.v17.i8.107437

Naunyn Schmiedebergs Arch Pharmacol. 2025 Sep 15. doi: 10.1007/s00210-025-04602-0. Online ahead of print.

NO ABSTRACT

PMID:40952477 | DOI:10.1007/s00210-025-04602-0

World J Stem Cells. 2025 Aug 26;17(8):111497. doi: 10.4252/wjsc.v17.i8.111497.

ABSTRACT

Bone marrow-derived mesenchymal stem cells (BMSCs) and adipose tissue-derived mesenchymal stem cells (ADSCs), two principal subtypes of mesenchymal stem cells with multilineage regenerative potential, have emerged as promising therapeutic strategies for various diseases. While BMSCs and ADSCs exhibit distinct functional profiles tailored to different therapeutic applications, emerging evidence suggests that ADSCs may be a more promising approach for treating ischemic pathologies, including myocardial infarction, ischemic stroke, and peripheral artery disease, in comparison with BMSCs. However, the precise molecular mechanisms by which ADSCs enhance the therapeutic outcomes in these diseases remain poorly understood. In this editorial, we comment on the article by Li et al, which systematically compares the therapeutic efficacy of ADSCs and BMSCs derived from the same elderly patients with coronary heart disease and explores the underlying mechanism from a metabolic perspective. This study proposes that the metabolite L-arginine in ADSCs isolated from elderly patients promotes angiogenesis and protects against apoptosis in a hypoxic and ischemic microenvironment, thereby enhancing myocardial repair following infarction. These findings not only highlight the metabolic plasticity of ADSCs but also position L-arginine as a pivotal therapeutic effector in coronary heart disease. Given the novel and crucial role of L-arginine in ischemic heart diseases, further exploration of L-arginine in ADSCs (particularly those derived from elderly individuals) is essential, including its roles in angiogenesis, cell death, and the potential therapeutic implications in other ischemic pathologies. Additionally, further investigation into additional metabolites in ADSCs is warranted to enhance the therapeutic potential of ADSCs in ischemic pathologies.

PMID:40951708 | PMC:PMC12427081 | DOI:10.4252/wjsc.v17.i8.111497

Drug Des Devel Ther. 2025 Sep 9;19:7929-7946. doi: 10.2147/DDDT.S515053. eCollection 2025.

ABSTRACT

Idebenone, a short-chain analog of coenzyme Q10 with a hydroxydecyl side chain, is known to activate mitochondrial function by transferring electrons to the electron transport chain complex III, thereby promoting adenosine triphosphate production. Numerous clinical trials have demonstrated the effectiveness of idebenone in the treatment of neurological diseases. Interestingly, emerging evidence suggests that idebenone may also have beneficial effects beyond neurological conditions through disrupting mitochondrial membrane potential, inducing mitochondrial apoptosis, promoting mitophagy attenuating ferroptosis, reducing reactive oxygen species and lipid peroxidation, etc. This study aims to comprehensively review the clinical potential of idebenone in various fields, including cancers (such as breast cancer, melanoma, glioblastoma, neuroblastoma, hepatocellular carcinoma, prostatic carcinoma and pancreatic carcinoma), cardiovascular diseases (including atherosclerosis, hypertension, myocardial infarction and heart failure), diabetes mellitus, liver diseases, urogenital diseases, sepsis, and other diseases. The findings highlight the potential of idebenone as a promising therapeutic option for the prevention and management of these condition, which need to be validated in more clinical trials.

PMID:40951694 | PMC:PMC12433227 | DOI:10.2147/DDDT.S515053

Food Sci Nutr. 2025 Sep 12;13(9):e70937. doi: 10.1002/fsn3.70937. eCollection 2025 Sep.

ABSTRACT

Exhaustive physical exercise, while promoting cardiovascular fitness, can paradoxically lead to excessive oxidative stress, systemic fatigue, and myocardial injury. Despite increasing awareness of exhaustion exercise myocardial damage, effective preventive strategies remain limited. Natural bioactive compounds with antioxidant and antiapoptotic properties have gained attention as potential interventions. Among them, triterpenoids derived from Ganoderma lucidum triterpenoids (GLTs) are notable for their potent free radical scavenging and cytoprotective effects. However, their cardioprotective potential under conditions of exhaustion exercise oxidative stress has not been fully elucidated. This study explores the antifatigue potential of GLTs and elucidates their underlying mechanisms through the establishment of a mouse model of exhaustion exercise via exhaustive treadmill running. This study showed that GLTs significantly alleviated exhaustion exercise by reducing serum fatigue biomarkers (CK, BUN, and LDH) and improving myocardial histopathological conditions. GLTs enhanced antioxidant capacity by decreasing MDA levels, increasing SOD and CAT activities, and elevating GSH content, thereby mitigating oxidative stress. Additionally, GLTs regulated apoptosis by downregulating Bax and Caspase-3 expression, upregulating Bcl-2 levels, and reducing the Bax/Bcl-2 ratio. Mechanistically, these effects were associated with activation of the Keap1/Nrf2/HO-1 signaling pathway. Collectively, this study provides new insights into the context-specific role of GLTs in protecting against exhaustion exercise myocardial injury. Our findings highlight the therapeutic potential of GLTs as a natural antioxidant strategy for mitigating oxidative stress, delaying fatigue, and preserving cardiac function under conditions of intensive physical exertion.

PMID:40951591 | PMC:PMC12431855 | DOI:10.1002/fsn3.70937

Narra J. 2025 Aug;5(2):e2245. doi: 10.52225/narra.v5i2.2245. Epub 2025 Apr 22.

ABSTRACT

Myocardial infarction (MI) is the leading cause of mortality worldwide. During MI, cardiomyocyte necrosis and inflammation are crucial in the post-MI cardiac remodeling process, including pyroptosis. Although colchicine is a well-known anti-inflammatory drug that has been clinically studied in the context of MI, its role in cardiac pyroptosis remains unclear. The aim of this study was to investigate the role of colchicine in pyroptosis in vitro, using CoCl2-induced H9c2 cells. Prior to the primary experiment, the hypoxic model in H9c2 cells was optimized by evaluating hypoxia-inducible factor-1 alpha (HIF-1α) expression and viability in cells exposed to various concentrations of CoCl2 at different time intervals. Subsequently, an in vitro hypoxia model was established by treating H9c2 cells with CoCl2 (600 µM), with or without colchicine (1 µM), for 3 hours. Flow cytometry was used to measure the expression of nuclear factor-kappa beta (NF-κB), interleukin 18 (IL-18), caspase-1, and HIF-1α in pyroptotic cells. Immunofluorescence was used to assess caspase-1 localization and its colocalization with propidium iodide during late-stage pyroptosis. Our data indicated that CoCl2-induced hypoxia significantly upregulated NF-κB, caspase-1, and IL-18 expression, and increased pyroptotic cell death in H9c2 cells. Colchicine treatment attenuated these effects, leading to a marked reduction in NF-κB, caspase-1, and IL-18 expression in hypoxic cells. Colchicine treatment significantly decreased the number of late pyroptotic cells. The protective effect of colchicine was more pronounced in late hypoxia (24-hour) setting compared to early hypoxia (3-hour). These findings suggest that colchicine attenuates cardiac pyroptosis in hypoxic H9c2 cells, as evidenced by the significant downregulation of key proteins involved in this pathway, including NF-κB, caspase-1, and IL-18. This protective effect appeared to be more effective in late hypoxia.

PMID:40951489 | PMC:PMC12425549 | DOI:10.52225/narra.v5i2.2245

Cureus. 2025 Aug 12;17(8):e89935. doi: 10.7759/cureus.89935. eCollection 2025 Aug.

ABSTRACT

Intravascular lithotripsy (IVL) delivers acoustic shockwaves to fracture coronary calcifications and optimize stent expansion, yet side branch (SB) occlusion after IVL is rarely documented. We report the case of an 80-year-old man with prior stents in the distal right coronary and proximal left circumflex arteries who underwent elective percutaneous coronary intervention for 75% proximal left anterior descending artery (LAD) stenosis supplying four diagonal branches: the first (D1), second (D2), third (D3), and fourth (D4) diagonal branches. The instantaneous wave-free ratio was 0.82 and the fractional flow reserve was 0.77, both indicating ischemia. Optical coherence tomography (OCT) demonstrated severe, long calcification (calcification score 4; maximum arc 330°; thickness 12.1 mm; length 38.2 mm; minimum lumen area 1.46 mm²), and IVL was selected over rotational atherectomy or scoring balloon angioplasty due to high calcification score and wire bias considerations. Eight cycles of IVL with a 2.5/12 mm balloon were applied from the D4 bifurcation to proximal LAD, followed by eight cycles with a 3.0/12 mm balloon, increasing the minimum lumen area to 3.31 mm². After pre-dilation with a 2.5/13 mm scoring balloon distally and a 3.0/15 mm non-compliant balloon proximally, a 2.5/38 mm everolimus-eluting stent was implanted, and the proximal segment was post-dilated with a 3.0/15 mm non-compliant balloon. Immediately after post-dilation, the patient developed chest pain and ST-segment elevation; angiography showed new occlusion of the third diagonal branch (D3, thrombolysis in myocardial infarction (TIMI) 0) and flow reduction in the first diagonal branch (D1) from TIMI 3 to TIMI 1, while all other branches maintained TIMI 3 flow. Wire recrossing and kissing balloon inflation (1.5/10 mm semi-compliant in D3, 3.0/15 mm non-compliant in the main vessel) restored TIMI 3 flow in D3 and relieved symptoms, whereas D1 remained TIMI 1 but asymptomatic. No protective wiring had been performed initially as the affected SB was <1.5 mm, but the subsequent ischemic event indicated it should be considered a significant branch. Angiography before and after IVL showed no change suggestive of SB risk, whereas OCT performed immediately after IVL revealed new protrusion of fractured calcifications into the D1 and D3 ostia, which was considered the cause of the subsequent side branch occlusion. IVL-related SB occlusion is an extremely rare complication in the literature, but meticulous pre-procedural OCT assessment and consideration of protective wiring in high-risk bifurcation lesions may help predict and prevent this event.

PMID:40951199 | PMC:PMC12425836 | DOI:10.7759/cureus.89935

FASEB Bioadv. 2025 Sep 12;7(9):e70049. doi: 10.1096/fba.2025-00187. eCollection 2025 Sep.

ABSTRACT

Myocardial infarction remains one of the leading causes of mortality. Reperfusion of the infarcted myocardium restores blood flow and reduces primary ischemic injury. However, despite its protective function, reperfusion is also associated with several deleterious outcomes that can result in ischemia-reperfusion (I/R) injury to cardiac tissue. Although negative outcomes such as reactive oxygen species generation are strongly associated with I/R injury, cardiac energy metabolism is also greatly disrupted. Furthermore, previous studies have shown that the restoration of normal fuel oxidation in the myocardium regulates the extent of contractile recovery. A better understanding of the pathophysiological mechanisms underlying I/R injury may allow us to develop new treatments that limit the negative aspects of the process. In this study, we examined the role played by GCN5L1, a protein implicated in the regulation of energy metabolism, in I/R injury. We demonstrate that cardiac-specific loss of GCN5L1 promotes the inhibitory phosphorylation of pyruvate dehydrogenase in vitro and in vivo, a process likely to inhibit glucose oxidation, and that this corresponds to increased myocardial damage following ischemia-reperfusion (I/R) injury.

PMID:40950650 | PMC:PMC12426763 | DOI:10.1096/fba.2025-00187

Am J Transl Res. 2025 Aug 15;17(8):6587-6600. doi: 10.62347/DODM6651. eCollection 2025.

ABSTRACT

OBJECTIVE: This study aimed to explore the mechanisms of Danqi Soft Capsules (DQ) in reducing myocardial ischemia/reperfusion injury (MI/RI) through network pharmacology, molecular docking, and experimental validation.

METHODS: The TCMSP database was used to screen for active ingredients of DQ and their potential targets, and compare them to MI/RI-related targets to construct a "drug-active ingredient-target" network. The protein-protein interaction (PPI) network was constructed using the STRING database; and Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. Molecular docking experiments verified the binding affinity between DQ's active ingredients and apoptosis-related target proteins, and cellular experiments validated DQ's anti-apoptotic effects in the H9c2 cardiomyocyte hypoxia/reoxygenation model.

RESULTS: Network pharmacology analysis identified 66 active ingredients and 240 potential targets, of which 105 were related to MI/RI. PPI network analysis screened out 10 core targets. GO and KEGG analyses indicated that these targets were related to the pathways of cell apoptosis. The molecular docking experiment confirmed that the active ingredient had a strong binding affinity with the core target, with the binding affinity between tumor necrosis factor (TNF) and tanshinone IIA being -9.2 kcal/mol, and that between tumor protein (TP) 53 and quercetin being -8.6 kcal/mol. Cellular experimental results showed that the cell apoptosis rate in the DQ-treated group was lower than in the model group, with the protective effect in the high-dose group being slightly better than the low-dose group.

CONCLUSION: This study revealed that DQ alleviates MI/RI by inhibiting cell apoptosis, providing a scientific basis for the clinical application of DQ and offering new directions for drug development.

PMID:40950270 | PMC:PMC12432725 | DOI:10.62347/DODM6651

bioRxiv [Preprint]. 2025 Sep 7:2025.09.02.673841. doi: 10.1101/2025.09.02.673841.

ABSTRACT

Late reperfusion therapy (LRT; ≥ 3 hours post-MI) significantly reduces the risk of ventricular rupture following myocardial infarction (MI), yet the structural and mechanical mechanisms behind this protection remain unclear. We hypothesized that LRT would alter the biomechanical properties of the infarct borderzone and to investigate this, we utilized laser micrometry, planar biaxial testing, and quantitative polarized light imaging (QPLI) to quantify spatial variations in the geometric, mechanical, and structural properties of the left ventricle extracellular matrix (LV ECM) in adult male Sprague-Dawley rats. Rats received permanent occlusion (PO), LRT, or a sham surgery and tissue was collected 1-day post-MI, during the inflammatory phase of healing. LRT generated a larger infarct borderzone (LRT: 31.5 ± 7.6 mm 2 ; PO: 22.5 ± 4.2 mm 2 ; p < 0.05) in comparison to PO. Infarct core and borderzone stiffness was reduced post-MI, and LRT samples exhibited smoother, more consistent stiffness gradients between infarct core and remote regions than PO samples. In general, infarcted LV ECM from were thicker and more spatially variable than sham samples, but less stiff. Additionally, dynamic QPLI revealed decreased collagen fiber alignment in infarct cores relative to borders, though this did not differ between PO and LRT groups. Complementary second harmonic generation imaging revealed more gradual, consistent transitions in collagen fiber alignment throughout LV ECMs subjected to LRT, although this was limited to one sample from each group. Ultimately, these results further justify LRT and may inform future therapeutic strategies aimed at spatially modulating post-MI tissue mechanics to improve patient outcomes.

PMID:40950054 | PMC:PMC12424736 | DOI:10.1101/2025.09.02.673841

World J Cardiol. 2025 Aug 26;17(8):107437. doi: 10.4330/wjc.v17.i8.107437.

ABSTRACT

Mesenchymal stem cells (MSCs) possess unique properties such as immunomodulation, paracrine actions, multilineage differentiation, and self-renewal. Therefore, MSC-based cell therapy is an innovative approach to treating various degenerative illnesses, including cardiovascular diseases. However, several challenges, including low transplant survival rates, low migration to the ischemic myocardium, and poor tissue retention, restrict the application of MSCs in clinical settings. These undesirable cell therapy outcomes mainly originated due to the overproduction of reactive oxygen species (ROS) in the injured heart. MSCs' stress-coping capacity can be enhanced by preconditioning them under conditions similar to the microenvironment of wounded tissues. Hydrogen peroxide (H2O2) is a ROS that has been shown to activate protective cellular mechanisms such as survival, proliferation, migration, paracrine effects, and differentiation at sublethal doses. These processes are induced via phosphatidylinositol 3-kinase/protein kinase B, p38 mitogen-activated protein kinases, c-Jun N-terminal kinase, Janus kinase/signal transducer and activator of the transcription, Notch1, and Wnt signaling pathways. H2O2 preconditioning could lead to many clinical benefits, including ischemic injury reduction, enhanced survival of cellular transplants, and tissue regeneration. In this review, we present an overview of stem cell preconditioning methods and the biological functions activated by H2O2 preconditioning. Furthermore, this review explores the molecular mechanisms underlying the protective cellular functions stimulated under H2O2 preconditioning.

PMID:40949936 | PMC:PMC12426982 | DOI:10.4330/wjc.v17.i8.107437

Ann Transl Med. 2025 Aug 31;13(4):40. doi: 10.21037/atm-25-27. Epub 2025 Aug 26.

ABSTRACT

BACKGROUND: Studies on light-elicited endothelial period circadian regulator 2 (PER2) mediated cardioprotection revealed a critical role of PER2/hypoxia inducible factor 1 alpha (HIF1A) regulated endothelial factor ANGPTL4 for endothelial barrier protection during myocardial ischemia and reperfusion injury (IRI). Based on these observations, we deepened our studies on light-elicited cardioprotective mechanisms.

METHODS: All animal and human studies had Institutional Animal Care and Use Committee (IACUC) and Colorado Multiple Institutional Review Board (COMIRB) approval. To study myocardial IRI, an in-situ mouse model for myocardial IRI was used. To study light-elicited mechanisms during myocardial IRI, endothelial-specific Per2-deficient mice were treated with the PER2 enhancer nobiletin (NOB), with the HIF1A activator dimethyloxalylglycine (DMOG), or with recombinant ANGPTL4. To evaluate whether light could increase ANGPTL4 or decrease troponin levels in patients, we exposed patients undergoing elective spine surgery postoperatively for 5 days with intense light for 30 minutes at sunrise. Patient's plasma samples were tested for melatonin, ANGPTL4 and troponin levels using enzyme-linked immunosorbent assay (ELISA).

RESULTS: The PER2 enhancer NOB or the HIF1A activator DMOG protected from myocardial IRI, which was abolished in endothelial-specific Per2-deficient mice. ANGPTL4 was able to overcome an endothelial Per2 deficiency and revealed protection during myocardial IRI in endothelial-specific Per2-deficient or control mice. Intense light therapy in patients undergoing non-cardiac surgery showed increased ANGPTL4 and decreased troponin plasma levels.

CONCLUSIONS: Our study demonstrates that only the PER2/HIF1A downstream target ANGPTL4 can overcome an endothelial Per2 deficiency. Moreover, we discovered that intense light therapy in patients following non-cardiac surgery can be used to increase plasma levels of the endothelial protective factor ANGTL4 and decrease troponin levels, an indicator of myocardial injury in non-cardiac surgery (MINS). Further research with larger, more diverse human cohorts and long-term follow-up is needed to validate these findings and develop targeted therapies.

PMID:40949684 | PMC:PMC12432674 | DOI:10.21037/atm-25-27

Front Pharmacol. 2025 Aug 29;16:1605363. doi: 10.3389/fphar.2025.1605363. eCollection 2025.

ABSTRACT

Dexmedetomidine (DEX) is a highly selective α2-Adrenergic Receptor (α2-AR) agonist which inhibits sympathetic nerve activity, and has been shown to have a wide range of sedative, analgesic, anesthetic and other effects, as well as reducing inflammation and exerting neuroprotective functions. Researches show that DEX provides an advantage of protecting vital organs from injury, such as myocardial, kidney or cerebral injury. Nowadays, the regulatory effect of DEX in ferroptosis has become a headline in current researches. Ferroptosis is a type of programmed cell death discovered in recent years and is considered to play an important role in mediating the onset and progression of diseases. The aim of this review is to further clarify the role and mechanism of DEX in inhibiting ferroptosis.

PMID:40949160 | PMC:PMC12425897 | DOI:10.3389/fphar.2025.1605363

Cardiovasc Diagn Ther. 2025 Aug 30;15(4):738-754. doi: 10.21037/cdt-2025-63. Epub 2025 Aug 7.

ABSTRACT

BACKGROUND: The association between hepatitis B virus (HBV) infection and cardiovascular disease (CVD) remains uncertain. This study aimed to investigate the impact of HBV infection on 13 major adverse cardiovascular events (MACEs) among patients with CVD with or without statin use.

METHODS: A prospective cohort study was conducted to examine the cardiovascular, metabolic [atherogenic index (AI) and atherogenic index of plasma (AIP)], hepatic [albumin-bilirubin index (ALBI) score and fibrosis 4 index (FIB-4)] and inflammatory parameters [complete blood count-derived inflammation indices (CBCIIs)] in patients with HBV-cardiovascular comorbidity. In total, 45,013 individuals participated in the baseline survey between June 2020 and August 2023 at The First Affiliated Hospital of Xi'an Jiaotong University. The patients were categorized into two groups according to their surface antigen status. Finally, a sample size of 496 participants was included in the study: patients with coexisting CVD and HBV (n=271) and patients with CVD alone (n=225). In hierarchical analyses, the Breslow-Day test assessed model conformance, while the Mantel-Haenszel test performed stratified Chi-squared testing. To control for potential confounders, logistic regression models estimated odds ratios (ORs) and 95% confidence intervals (CIs) for MACEs.

RESULTS: HBV infection served as a protective factor of coronary heart disease (CHD) (OR =0.27; 95% CI: 0.12-0.60; P=0.001) and angina pectoris (AP) (OR =0.56; 95% CI: 0.36-0.86; P=0.008). Conversely, HBV infection elevated the risk of acute myocardial infarction (AMI) (OR =2.24, 95% CI: 1.40-3.57; P=0.001). Our study also suggests that statin therapy can lead to a dose-dependent decrease in liver fibrosis, and an increase in the atherogenicity index and systemic inflammatory response among patients with CVD.

CONCLUSIONS: Our findings suggest that patients with CVD who also have HBV infection may experience a reduction in MACEs when treated with statins. The observed improvements in hepatic function, atherosclerotic burden, and systemic inflammation associated with statin therapy may contribute to the favorable cardiovascular outcomes among individuals with CVD. This study demonstrates that in CVD patients infected with HBV, concurrent monitoring of metabolic and inflammatory parameters can help reduce the risk of MACEs. Future studies will focus on determining quantitative relationships between individual metabolic or inflammatory indicators and MACEs in larger cohorts.

PMID:40948721 | PMC:PMC12432611 | DOI:10.21037/cdt-2025-63

Pediatr Res. 2025 Sep 15. doi: 10.1038/s41390-025-04390-6. Online ahead of print.

NO ABSTRACT

PMID:40954232 | DOI:10.1038/s41390-025-04390-6

Ann Thorac Surg. 2025 Sep 13:S0003-4975(25)00877-X. doi: 10.1016/j.athoracsur.2025.08.047. Online ahead of print.

ABSTRACT

BACKGROUND: Understanding center performance in congenital heart surgery remains challenging, with limitations to standard regression approaches. Modern causal inference methods may improve estimation of expected mortality through better balancing case-mix but have not been studied.

METHODS: Benchmark operations (BMO) across 115 centers (2016-2022) from the STS Congenital Database were included. The standard approach uses mixed-effects logistic regression to estimate center's expected operative mortality inclusive of all patients, even those treated at the center of interest ("target") and those from other centers regardless of how closely aligned with the target. The causal approach creates tailored comparison groups, including only like patients from other centers using weights. We used three different weights (entropy balancing [EBW], stable balancing [SBW], covariate balancing propensity score [CBPS]) and compared to standard regression.

RESULTS: Among 42,579 BMO, overall operative mortality was 2.37%. Centers' mean [25th, 75th] regression-based expected mortality was lower (2.03% [1.42%, 2.58%]) than weighted estimates (EBW=2.10% [1.64%, 2.67%]; SBW=2.09% [1,57%, 2.69%]; CBPS=2.10% [1.63%, 2.66%]) and less variable. The mean ratio of weighted to regression mortality estimate was 1.03 for all estimates, with 25th and 75th percentiles: EBW [0.89, 1.16]; SBW [0.87, 1.15]; and CBPS [0.92, 1.17]. The distributions of operation type and other risk factors were better aligned with the target center in weighted estimates. The largest differences among methods were observed at smaller volume centers.

CONCLUSIONS: Causal inference methods constructed more tailored comparison groups for estimating center's expected mortality, with better alignment of case-mix. Adoption of newer approaches may be warranted.

PMID:40953790 | DOI:10.1016/j.athoracsur.2025.08.047

J Thorac Cardiovasc Surg. 2025 Sep 13:S0022-5223(25)00770-6. doi: 10.1016/j.jtcvs.2025.08.049. Online ahead of print.

ABSTRACT

BACKGROUND: The Ross procedure is a well-established option for aortic valve replacement, although progressive autograft dilation remains a significant long-term complication. While several reinforcement techniques have been proposed to address this issue, their effectiveness has yet to be rigorously evaluated.

METHODS: A PRISMA-compliant search was conducted for studies involving reinforced (RR) and non-reinforced (NR) Ross procedures. Meta-analysis with individual patient data (IPD) assessed survival and freedom-from-autograft reoperation rates. Subgroup analyses were conducted for the various reinforcement methods.

RESULTS: Sixteen cohort studies comprising 2,514 reinforced Ross (RR) and 595 non-reinforced (NR) patients were included. Pre- and peri-operative characteristics were comparable between groups. Individual patient data analysis of comparative studies demonstrated superior survival in the RR group, with 5-, 10-, and 15-year survival rates of 100%, 98.8%, and 98.8%, respectively, compared to 95.0%, 93.7%, and 82.6% in the NR group (HR: 11.9, p=0.016). Similarly, freedom from autograft reoperation at 5, 10, and 15 years was 96.4%, 94.2%, and 86.6% in the RR group versus 95.8%, 87.6%, and 77.7% in the NR group (HR: 2.06, p<0.001). Subgroup analysis showed comparable outcomes across different reinforcement techniques.

CONCLUSIONS: Reinforced Ross procedures are associated with improved survival and freedom-from-autograft reoperation rates compared to unsupported pulmonary autografts.

PMID:40953744 | DOI:10.1016/j.jtcvs.2025.08.049