Results 21 to 30 of about 178,200 (246)

Tumor Extracellular Vesicles Aggravate Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury

Advanced Science, EarlyView.
This study reveals a novel mechanistic connection between cancer and ischemia/reperfusion (I/R)‐induced cardiac injury. The meta‐analysis demonstrates significantly higher incidence ratios of both all‐cause mortality and cardiovascular mortality in cancer patients undergoing percutaneous coronary intervention (PCI) compared to non‐cancer patients.
Zhongting Mei, Qian Liu, Guoxin Liu, Manjie Zhang, Jiaxin Fang, Xuting He, Xueqi He, Zhengwei Qin, Ronghua Liu, Chuang Liu, Hongyu Ji, Yuechao Dong, Ye Yuan, Baofeng Yang, Weijie Du   +14 more
wiley   +1 more source

Irisin Attenuates Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension via Ubiquitin‐Mediated Regulation of ENO1

Advanced Science, EarlyView.
Irisin is a crucial plasma biomarker and promising therapeutic target that reflects disease severity, pulmonary vascular remodeling status and clinical outcome in patients with pulmonary arterial hypertension (PAH). As a novel protective factor, irisin is downregulated in PAH. By ubiquitination, irisin promotes Enolase 1 degradation and suppresses cell
Na Sun, Yong‐Bing Wang, Jing Huang, Run‐Wei Deng, Hui‐Yu He, Lei Gao, Xuan Gao, You‐Li Fan, Yan Cong, Yao‐Lei Guo, Yi‐Qiang Chen, Gui‐Jia Wang, Shao‐Hong Fang, Xia Gu, Bo Yu, Bing‐Xiang Wu   +15 more
wiley   +1 more source

Gut Metabolite Indole‐3‐Propionic Acid Regulates Macrophage Autophagy Through PPT1 Inhibiting Aging‐Related Myocardial Fibrosis

Advanced Science, EarlyView.
IPA is an intestinal tryptophan metabolite whose effects decline with decreased heart function. Supplementing IPA can alleviate the aging‐related myocardial fibrosis through PPT1. PPT1 is a key protein localized to lysosomes, and IPA can restore macrophage autophagy function by regulating PPT1 expresssions, thereby reducing aging‐related myocardial ...
Jing Lu, Hongyan Wang, Haiyu Zhang, Jiahao Li, Hanqi Li, Qiuyu Chen, Dongyu Han, Jialiang Liu, Lin Lv, Jie Xiong, Keying Yuan, Xianpeng Wei, Siqi Sheng, Fukai Liu, Yuanqi Shi, Zengxiang Dong, Yue Li   +16 more
wiley   +1 more source

Cardiovascular Disease Meets Cancer: Exploring the Epidemiology in China and Homotherapy Targeting Intersectional Mechanisms

Advanced Science, EarlyView.
Cardiovascular disease (CVD) and cancer are leading causes of death worldwide, with overlapping risk factors and pathophysiological mechanisms. This review explores shared pathways, including metabolic dysregulation, chronic inflammation, and gut microbiome alterations, highlighting dual‐benefit strategies such as lifestyle modifications and repurposed
Shihan Xiang, Yujie Shan, Shihong Xu, Jing Wang, Meng Luo, Jiaojiao Zhou, Qishan Chen   +6 more
wiley   +1 more source

Diastolic Dysfunction and Heart Failure

Journal of the American College of Cardiology, 2007
I would like to congratulate Dr. Persson and colleagues for their recently published echocardiographic substudy of the CHARM (Candesartan in Heart Failure—Assessment of Reduction in Mortality and Morbidity)-Preserved trial ([1][1]).
openaire   +3 more sources

The GRK2/AP‐1 Signaling Axis Mediates Vascular Endothelial Dysfunction and Atherosclerosis Induced by Oscillatory Low Shear Stress

Advanced Science, EarlyView.
This study highlights GRK2 is a central mediator in OSS‐induced endothelial dysfunction. OSS activates GPCRs in endothelial cells, leading to GRK2 phosphorylation and the activation of AP‐1. AP‐1 induces inflammation, while also promoting NR4A1 expression and anchoring LKB1 in the nucleus, which suppresses AMPK activity. This cascade causes endothelial
Li‐Da Wu, Yi Shi, Chao‐Hua Kong, Ai‐Qun Chen, Ying Kang, Jun‐Yan Kan, Xiao‐Min Jiang, Peng Chu, Dong‐Chen Wang, Yi‐Fei Lv, Zhi‐Yuan Qian, Zi‐Hao Jiang, Yun‐Wei Chen, Yue Sun, Rui‐Rui Chang, Wen‐Ying Zhou, Yue Gu, Jun‐Xia Zhang, Shao‐Liang Chen   +18 more
wiley   +1 more source

Mesencephalic Astrocyte‐Derived Neurotrophic Factor Binds BAX to Preserve Mitochondrial Homeostasis and Energy Metabolism for Relieving Myocardial Hypertrophy

Advanced Science, EarlyView.
MANF in cardiomyocytes interacts with BAX to impede BAX mitochondrial translocation and cytochrome c release, further stabilizing mitochondrial structure and energy supply to relieve myocardial apoptosis and hypertrophy, which indicates MANF as a novel cardioprotective factor to have a promising clinical application for myocardial hypertrophy ...
Dong Wang, Xinru Zhang, Baolong Wang, Haipeng Li, Dongshuo Xu, Yun Yang, Jialu Zhang, Wenbing Wang, Ren Zhang, Xinyu Wang, Yunfeng Cai, Shiyu Cao, Chao Hou, Changhui Wang   +13 more
wiley   +1 more source

CD74 Blockade Disrupts Endothelial Migrasome Signaling to Prevent Inflammatory Macrophage Differentiation and Inhibit Atherosclerotic Progression

Advanced Science, EarlyView.
Migrasomes play a crucial role in endothelial‐immune interactions in atherosclerosis. This study identifies migrasomes as amplifiers in the inflammatory cascade, driving immune‐metabolic reprogramming via “migrasome‐APP‐CD74” signaling. Blocking CD74 disrupts migrasome‐mediated signaling, attenuating atherosclerosis progression.
Kangnan Zhang, Jiong Chen, Zhenhua Zhu, Hong Hu, Qinghui Zhang, Rongrong Jia, Na Wang, Shihao Xiang, Yong Zhou, Yuehong Wang, Ling Xu   +10 more
wiley   +1 more source

The Role of HINT3 in Myocardial Ischemia‐Reperfusion Injury in Male Mice: Mechanisms Involving SDHA and its Acetylation

Advanced Science, EarlyView.
HINT3 expression declines after myocardial ischemia‐reperfusion injury. In male mice, loss of HINT3 worsens cardiac injury and mitochondrial dysfunction, while its overexpression is protective. HINT3 binds the mitochondrial enzyme succinate dehydrogenase (SDHA) and prevents its deacetylation by histone deacetylase 1 (HDAC1), reducing succinate ...
Jiabin Yu, Qi Yao, Tongtong Hu, Yadan Zhang, Ying Liu, Yang Xiao, Qingqing Wu, Qizhu Tang   +7 more
wiley   +1 more source

Diastolic Dysfunction and Doppler Echocardiography

Journal of the American College of Cardiology, 2005
The recent review by Maurer et al. ([1][1]) on diastolic dysfunction was a welcome read. I concur completely with their observations that “have led us to fundamentally question whether diastolic dysfunction is the underlying pathologic mechanism of the heart failure syndrome in all ...
openaire   +3 more sources