Corrigendum to "Ferroptosis in heart failure" [Journal of Molecular and Cellular Cardiology, Volume 173 (2022) Pages 141-153] [0.03%]
关于“心力衰竭中铁死亡的的作用”一文的勘误(《分子和细胞心脏病学杂志》第173卷(2022年)第141-153页)
Xinquan Yang,Nicholas K Kawasaki,Junxia Min et al.
Xinquan Yang et al.
Pathophysiology and pharmacotherapy of cardiovascular complications in metabolic syndrome [0.03%]
代谢综合征患者心血管并发症的病理生理及药物治疗
Naranjan S Dhalla,Chigar A Patel,Jayesh V Beladiya et al.
Naranjan S Dhalla et al.
Metabolic syndrome (MetS) symbolises a cluster of interrelated risk factors including central obesity, dyslipidemia, insulin resistance and hypertension, those significantly increase the risk of cardiovascular diseases (CVD). Individuals wi...
Small-molecule cocktail 5SM induces heart regeneration by upregulating TGFβ/BMP signaling [0.03%]
小分子鸡尾酒5SM通过上调TGFβ/BMP信号诱导心脏再生
Yuanyuan Chen,Lixia Zheng,Connie Xiong et al.
Yuanyuan Chen et al.
Zebrafish and neonatal mammals possess a remarkable capacity for cardiac regeneration following injury, a property that is largely absent in adult mammals. We have recently identified a cocktail of five small molecules (5SM) that promote ad...
OSK-mediated partial reprogramming induces cardiomyocyte dedifferentiation, overcomes cytokinesis barriers, and promotes post-MI endogenous cardiac regeneration [0.03%]
通过OSK介导的部分重编程促进心肌细胞去分化、克服胞质分裂障碍并促进心梗后内源性心脏再生
Yaobin Yan,Yingbo Huang,Changchang Cao et al.
Yaobin Yan et al.
Myocardial infarction (MI) leads to irreversible loss of cardiomyocytes (CMs), owing to the limited regenerative capacity of the adult mammalian heart. Previous studies indicate that the Yamanaka factors (OSKM) can induce CM dedifferentiati...
Phospho-mimic βIII-tubulin rescues microtubule and cardiac defects in Duchenne muscular dystrophy mice [0.03%]
磷酸模拟βIII-微管蛋白可修复杜氏肌营养不良小鼠的微管和心脏缺陷
Delong Zhou,Julie Nouet,Elam Mesa et al.
Delong Zhou et al.
Duchenne muscular dystrophy (DMD) cardiomyopathy is caused by mutations in the dystrophin gene and characterized by profound cytoskeletal disorganization, particularly pathological remodeling of the cardiomyocyte microtubule network. While ...
Junctophilin-2 abundance is unaltered in human heart failure samples with disrupted T-tubules and contractility [0.03%]
人类心脏 Failure样本中的-Junctophilin-2含量在T小管结构和功能紊乱时保持不变
Fotios Pitoulis,Blanca Pamias-Lopez,Kenneth Bedi et al.
Fotios Pitoulis et al.
T-tubules are structural components of the cardiomyocyte plasma membrane that are imperative for efficient excitation-contraction coupling and cardiac contraction. Junctophilin-2 (JPH2) has been postulated in multiple preclinical models to ...
Evolutionary differentiation of duplicated hoxb5 paralogs orchestrates calcium signaling and contractility [0.03%]
进化分化出的重复hoxb5同源物调节钙信号传导和收缩力
Yao Zu,Haiwang Jia,Bingqi Wang et al.
Yao Zu et al.
hox genes are evolutionarily conserved transcription factors essential for anterior-posterior body patterning, yet their specific contributions to cardiac morphogenesis and calcium signaling remain elusive. Using zebrafish as a model for ve...
CYLD-mediated DNA damage coordinates pathological cardiac hypertrophy via RIPK1-dependent signaling [0.03%]
CYLD介导的DNA损伤通过RIPK1依赖性信号通路协调病理性心脏肥大反应
Xianyun Jiang,Mengyuan Shi,Jiamin Guo et al.
Xianyun Jiang et al.
Cardiac remodeling under pressure overload involves maladaptive changes that lead to heart failure. This study investigated the role of the deubiquitinating enzyme CYLD in this process. We found that CYLD expression was significantly upregu...
Corrigendum to 'NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis' [Journal of Molecular and Cellular Cardiology 102 (2017) 10-21] [0.03%]
“NADPH氧化物酶4调节衰老和动脉粥样硬化中的血管炎症”[《分子与细胞心脏病学杂志》102卷（2017）10-21页]的勘误表
Andrey Lozhkin,Aleksandr E Vendrov,Hua Pan et al.
Andrey Lozhkin et al.
A review of peroxisome biology: Potential implications for cardiac physiology and pathology [0.03%]
过氧化物酶体生物学的回顾：对心脏生理和病理的潜在影响
Pukjera J Rungreang,Sean Noudali,Erik A Blackwood et al.
Pukjera J Rungreang et al.
The human heart has often been described as the "metronome of life" beating continuously over 2.5 billion times across the average lifespan and consuming more than 6 kg of ATP daily. And, during both a healthy and diseased state, the heart ...