Results 41 to 50 of about 180,059 (262)

Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors

Frontiers in Cardiovascular Medicine, 2022
Cardiac hypertrophy is a key process in cardiac remodeling development, leading to ventricle enlargement and heart failure. Recently, studies show the complicated relation between cardiac hypertrophy and epigenetic modification.
Yu Han, Yu Han, Jiali Nie, Jiali Nie, Dao Wen Wang, Dao Wen Wang, Li Ni, Li Ni   +7 more
doaj   +1 more source

SR‐A3 Promotes USP18‐Mediated deISGylation of STING to Protect Against Myocardial Ischemia‐Reperfusion Injury

Advanced Science, EarlyView.
MI/RI is a major clinical challenge with high morbidity and mortality. This study demonstrates that SR‐A3 expression is downregulated in MI/RI, and its deletion exacerbates damage via the USP18/ISG15/STING axis, revealing SR‐A3 as a potential therapeutic target.
Yufei Han, Guolin Miao, Yinqi Zhao, Zhiyong Du, Kaikai Lu, Changqi Xiao, Aiden Xian, Jiaxin Duanmu, Zihao Zhou, Jinxuan Chen, Lianxin Zhang, Chao Zhai, Yitong Xu, Zhaoling Li, Xianqin Shen, Sijing Shi, Jingxuan Chen, Si Mei, Yuan Fang, Liwen Zheng, Ling Zhang, Yuhui Wang, Wei Huang, Erdan Dong, Xunde Xian   +24 more
wiley   +1 more source

KLF5 Downregulation Links Impaired BNIP3‐Mediated Mitophagy to Inflammatory Valve Remodeling in Calcific Aortic Valve Disease

Advanced Science, EarlyView.
In human CAVD, KLF5 is reduced in VIC‐rich regions and remodeling/stress‐associated VIC states. In VICs, KLF5 sustains BNIP3 promoter activity and BNIP3‐mediated mitophagy, thereby limiting cytosolic mtDNA accumulation. KLF5 loss weakens mitochondrial quality control and enhances mtDNA‐sensitive STING/NF‐κB/NLRP3 inflammatory signaling under osteogenic
Jin‐Hui Bian, Jia‐Xi Gu, Zhang Yue, Chun‐Ze Yuan, Hai‐Bin Ji, Ao Li, Yu Zhong, Xiu‐Fan Xu, Yu‐Qiu He, Ye‐Fan Jiang, Hong‐Shan Chen, Xiang Chen, Meng‐Lin Chao, Yong‐Feng Shao   +13 more
wiley   +1 more source

ANGPTL8 is a negative regulator in pathological cardiac hypertrophy

Cell Death and Disease, 2022
Pathological cardiac hypertrophy is an independent risk factor for heart failure and is considered a target for the treatment of heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown.
Lin Hu, Jiarui Wei, Yue Zhang, Ziyuan Wang, Junming Tang, Jian Tang, Yujiu Gao, Xiaoqiao Zhang, Yifan Li, Yantong Liu, Shinan Ma, Xingrong Guo, Qiufang Zhang   +12 more
doaj   +1 more source

SerpinA3 is an Endogenous TGF‐β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling

Advanced Science, EarlyView.
SerpinA3 acts as an endogenous TGF‐β receptor antagonist that binds to the extracellular domain of TGFR‐1, thereby preventing TGFR‐1–TGFR‐2 complex formation. This receptor‐level blockade suppresses TGF‐β/Smad2/3 signaling, attenuates cardiac fibroblast activation, and extracellular matrix deposition, and ultimately alleviates pressure overload–induced
Hui Wang, Jieyu Cui, Chunlu Huang, Wanyi Guo, Tong Liu, Yi Zhu, Shuai Shao, Kangyin Chen, Jinlong He, Qiankun Bao   +9 more
wiley   +1 more source

Quercetin Attenuates Cardiac Hypertrophy by Inhibiting Mitochondrial Dysfunction Through SIRT3/PARP-1 Pathway

Frontiers in Pharmacology, 2021
Cardiac hypertrophy is an important characteristic in the development of hypertensive heart disease. Mitochondrial dysfunction plays an important role in the pathology of cardiac hypertrophy.
Wen-Jing Chen, Wen-Jing Chen, Yan Cheng, Wen Li, Xiao-Kang Dong, Jian-liang Wei, Chuan-Hua Yang, Yue-Hua Jiang   +7 more
doaj   +1 more source

Periostin‐CCL3 Feedforward Signaling Loop Promotes Cardiac Fibrosis and Cardiomyocyte Necroptosis in Arrhythmogenic Cardiomyopathy

Advanced Science, EarlyView.
POSTN‐CCL3 signaling forms a feed‐forward circuit between cardiomyocytes and cardiac myofibroblasts in arrhythmogenic cardiomyopathy. POSTN activates JNK/RIP3‐dependent necroptotic signaling and JNK/ETS2‐induced CCL3 expression in cardiomyocytes. In turn, CCL3‐CCR5 signaling in cardiac myofibroblasts activates NF‐κB/p65 and promotes POSTN expression ...
Tiantian Wu, Ruotong Li, Xiaoyue Zhang, Dandan Chen, Jianmeng Yang, Mengmeng Li, Yuhan Yin, Ya Wang, Yuqiu Tian, Haoling Yan, Dan Cui, Jiangping Song, Gaoliang Ouyang   +12 more
wiley   +1 more source

JNK signaling-dependent regulation of histone acetylation are involved in anacardic acid alleviates cardiomyocyte hypertrophy induced by phenylephrine.

PLoS ONE, 2021
Cardiac hypertrophy is a complex process induced by the activation of multiple signaling pathways. We previously reported that anacardic acid (AA), a histone acetyltransferase (HAT) inhibitor, attenuates phenylephrine (PE)-induced cardiac hypertrophy by ...
Bohui Peng, Chang Peng, Xiaomei Luo, Shuqi Wu, Qian Mao, Huanting Zhang, Xiao Han   +6 more
doaj   +1 more source

Computational models of cardiac hypertrophy

Progress in Biophysics and Molecular Biology, 2021
Cardiac hypertrophy, defined as an increase in mass of the heart, is a complex process driven by simultaneous changes in hemodynamics, mechanical stimuli, and hormonal inputs. It occurs not only during pre- and post-natal development but also in adults in response to exercise, pregnancy, and a range of cardiovascular diseases.
Kyoko Yoshida, Jeffrey W. Holmes
openaire   +3 more sources

An Extracellular Pore‑Targeting Peptide Defines a Designable Allosteric Site in TRPV2

Advanced Science, EarlyView.
Structure‐guided peptide engineering yields Depiv2, a highly potent and subtype‐selective TRPV2 inhibitor that binds to the extracellular pore and remodels it into a closed, non‐conductive state. Depiv2 suppresses pathological cardiac hypertrophy, establishing the TRPV2 outer pore as a designable interface for selective peptide modulation.
Aiqin Zhu, Hongkun Wang, Jiawei Wang, Xiaolu Liu, Aerziguli Aierken, Lizhen Xu, Ping Liang, Fan Yang   +7 more
wiley   +1 more source