Abnormal succinate accumulation aggravates heart failure via the SUCNR1-Smad2/3-PDK1 pathway

Mendeley Data2026-04-09 收录

心脏衰竭病理机制

SUCNR1-PDK1信号通路

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Abnormal succinate accumulation aggravates heart failure via the SUCNR1-Smad2/3-PDK1 pathway

异常琥珀酸堆积通过SUCNR1-Smad2/3-PDK1通路加重心力衰竭

Table_1_Role of Endothelial and Mesenchymal Cell Transitions in Heart Failure and Recovery Thereafter.XLS

心脏衰竭病理机制

细胞命运转变

Background: Mechanisms of myocardial recovery are not well elucidated. Methods: 3-month-old C57/BL6 mice were treated with Angiotensin-II infusion and N (w)-nitro-L-arginine methyl ester in drinking w

NIAID Data Ecosystem50

Characteristics of gene expression in epicardial adipose tissue and subcutaneous adipose tissue in patients at risk for heart failure undergoing coronary artery bypass grafting

心脏衰竭病理机制

脂肪组织基因表达

Characteristics of gene expression in epicardial adipose tissue and subcutaneous adipose tissue in patients at risk for heart failure undergoing coronary artery bypass grafting

ChEBI2024-09-09 更新10

Data_Sheet_1_Ca2+/Calmodulin-Dependent Protein Kinase II Regulation by RIPK3 Alleviates Necroptosis in Transverse Arch Constriction-Induced Heart Failure.XLSX

心脏衰竭病理机制

坏死性凋亡调控

Some studies have reported that the activation of Ca2+/calmodulin dependent protein kinase (CaMKII) plays a vital role in the pathogenesis of cardiovascular disease. Moreover, receptor interacting pro

NIAID Data Ecosystem10

p53-dependent mitochondrial compensation in heart failure with preserved ejection fraction

心脏衰竭病理机制

线粒体功能障碍

BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) accounts for 50% of heart failure patients. Clinically, HFpEF prevalence show age and gender biases. Although the majority of HFpEF p

NIAID Data Ecosystem50

Modulation of miR-29 influences myocardial compliance likely through coordinated regulation of calcium handling and extracellular matrix

心脏衰竭病理机制

基因治疗靶点

MicroRNAs (miRs) control the expression of diverse subsets of target mRNAs, and studies have found miR dysregulation in failing hearts. Expression of miR-29 is abundant in heart, increased with aging,

NIAID Data Ecosystem10

Abnormal succinate accumulation aggravates heart failure via the SUCNR1-Smad2/3-PDK1 pathway

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