Acupoint catgut embedding alleviates experimental autoimmune encephalomyelitis by modulating neuroinflammation and potentially inhibiting glia activation through JNK and ERK pathways.

Background: Acupoint catgut embedding (ACE) is a traditional Chinese medicine technique commonly used for managing various disorders, including chronic inflammatory pain and allergic asthma. Despite its growing use, the neuroimmunological mechanisms underlying ACE treatment effects remain unclear.

Methods: This study investigated the roles and potential mechanisms of the effects of ACE in treating experimental autoimmune encephalomyelitis (EAE), a frequently used animal model of autoimmune neuroinflammation.

Performance of Subcutaneous Implantable Cardioverter Defibrillator (S-ICD) in Chinese Population with Primary Prevention Indications: A Prospective Observational Cohort Study.

BACKGROUND International studies have shown that use of a subcutaneous implantable cardioverter defibrillator (S-ICD) could reduce lead-related complications while maintaining adequate defibrillation performance; however, data from the Chinese population or other Asian groups are limited. MATERIAL AND METHODS SCOPE is a prospective, multicenter, observational cohort study. Two hundred patients with primary prevention indication for sudden cardiac death (SCD), who are candidates for S-ICD, will be enrolled.

Semaphorin‑3A alleviates cardiac hypertrophy by regulating autophagy.

Cardiac hypertrophy, characterized by cardiomyocyte enlargement, is an adaptive response of the heart to certain hypertrophic stimuli; however, prolonged hypertrophy results in cardiac dysfunction and can ultimately cause heart failure. The present study evaluated the role of semaphorin-3A (Sema3A), a neurochemical inhibitor, in cardiac hypertrophy, utilizing an isoproterenol (ISO) induced H9c2 cell model. Cells were stained with rhodamine-phalloidin to assess the cell surface area and reverse transcription-quantitative PCR was performed to quantify mRNA expression levels of Sema3A, brain natriuretic factor (BNF) and β-myosin heavy chain (β-MHC).

GSK2795039 prevents RIP1-RIP3-MLKL-mediated cardiomyocyte necroptosis in doxorubicin-induced heart failure through inhibition of NADPH oxidase-derived oxidative stress.

Doxorubicin (DOX), which is widely used for the treatment of cancer, induces cardiomyopathy associated with NADPH oxidase-derived reactive oxygen species. GSK2795039 is a novel small molecular NADPH oxidase 2 (Nox2) inhibitor. In this study, we investigated whether GSK2795039 prevents receptor-interacting protein kinase 1 (RIP1)-RIP3-mixed lineage kinase domain-like protein (MLKL)-mediated cardiomyocyte necroptosis in DOX-induced heart failure through NADPH oxidase inhibition.

Sphingosine-1-phosphate induces myocyte autophagy after myocardial infarction through mTOR inhibition.

Sphingosine-1-phosphate (S1P)/S1P receptor 1 signaling exerts cardioprotective effects including inhibition of myocyte apoptosis. However, little is known about the effect of S1P treatment on myocyte autophagy after myocardial infarction (MI). In the present study, we tested the hypothesis that S1P induces myocyte autophagy through inhibition of the mammalian target of rapamycin (mTOR), leading to improvement of left ventricular (LV) function after MI.

Apocynin prevents reduced myocardial nerve growth factor, contributing to amelioration of myocardial apoptosis and failure.

Reduced nerve growth factor (NGF) is associated with cardiac sympathetic nerve denervation in heart failure (HF) which is characterized by increased oxidative stress. Apocynin is considered an antioxidant agent which inhibits NADPH oxidase activity and improves reactive oxygen species scavenging. However, it is unclear whether apocynin prevents reduced myocardial NGF, leading to improvement of cardiac function in HF.

Comparison of infarction size, complete ST-segment resolution incidence, mortality and re-infarction and target vessel revascularization between remote ischemic conditioning and ischemic postconditioning in ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.

Introduction: Due to higher morbidity and mortality, ST-segment elevation myocardial infarction (STEMI) causes many public health problems.

Aim: To observe effects of remote ischemic conditioning (RIC) and ischemic postconditioning (IPC) on patients diagnosed as STEMI undergoing primary percutaneous coronary intervention (pPCI).

Material And Methods: This meta-analysis was conducted using indirect comparison by conducting a network meta-analysis (NMA).

The NADPH oxidase inhibitor apocynin improves cardiac sympathetic nerve terminal innervation and function in heart failure.

New Findings: What is the central question of this study? Does NADPH oxidase activation mediate cardiac sympathetic nerve denervation and dysfunction in heart failure. What is the main findings and its importance? Cardiac sympathetic nerve terminal density and function were reduced in heart failure after myocardial infarction in rabbits. The NADPH oxidase inhibitor apocynin prevented the reduction in cardiac sympathetic nerve terminal density and function in heart failure.

CAMI-NSTEMI Score - China Acute Myocardial Infarction Registry-Derived Novel Tool to Predict In-Hospital Death in Non-ST Segment Elevation Myocardial Infarction Patients.

Background: Accurate risk stratification of non-ST segment elevation myocardial infarction (NSTEMI) patients is important due to great variability in mortality risk, but, to date, no prediction model has been available. The aim of this study was therefore to establish a risk score to predict in-hospital mortality risk in NSTEMI patients.

Methods and results: We enrolled 5,775 patients diagnosed with NSTEMI from the China Acute Myocardial Infarction (CAMI) registry and extracted relevant data.

Oxidative stress impairs myocyte autophagy, resulting in myocyte hypertrophy.

New Findings: What is the central question of this study? Does oxidative stress induce impairment of autophagy that results in myocyte hypertrophy early after pressure overload? What is the main finding and its importance? In cultured myocytes, hydrogen peroxide decreased autophagy and increased hypertrophy, and inhibition of autophagy enhanced myocyte hypertrophy. In rats with early myocardial hypertrophy after pressure overload, myocyte autophagy was progressively decreased. The antioxidant N-acetyl-cysteine or the superoxide dismutase mimic tempol prevented the decrease of myocyte autophagy and attenuated myocyte hypertrophy early after pressure overload.

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling.

Background/aims: The alterations in myocyte autophagy after myocardial infarction (MI) and the underlying mechanisms have not been fully understood. In this study, we investigated the temporal changes of myocyte autophagy in the remote non-infarcted myocardium in rabbits after MI and the relationships between alterations of myocyte autophagy and left ventricular (LV) remodeling and myocardial oxidative stress.

Methods: Rabbits were assigned to MI or sham operation.

Distinct changes of myocyte autophagy during myocardial hypertrophy and heart failure: association with oxidative stress.

What is the central question of this study? We investigated the changes of myocyte autophagy during the stages of myocardial hypertrophy and failure and the relationship between autophagy and oxidative stress. What is the main findings and its importance? Myocyte autophagy is reduced during myocardial hypertrophy and increased during heart failure. Reduced autophagy is correlated with myocyte hypertrophy, and increased autophagy is correlated with myocyte apoptosis.