Filtered By:
Condition: Heart Disease
This page shows you your search results in order of date. This is page number 3.
Order by Relevance | Date
Total 126 results found since Jan 2013.
MicroRNA-223-3p promotes pyroptosis of cardiomyocyte and release of inflammasome factors via downregulating the expression level of SPI1 (PU.1)
Toxicology. 2022 Jul 2:153252. doi: 10.1016/j.tox.2022.153252. Online ahead of print.ABSTRACTDiabetic cardiomyopathy (DCM) is a common heart disease in patients with diabetes mellitus (DM), and is sometimes its main cause of death. Among all the causes of DCM, myocardial cell death is considered to be the most basic pathological change. Furthermore, studies have shown that pyroptosis, the pro-inflammatory programmed cell death, contributes to the progress of DCM. MicroRNAs (miRNAs) also have been proved to take part in the formation of DCM. However, it is not clear whether and how miRNAs regulate myocardial cell pyroptosis...
Source: Toxicology - July 6, 2022 Category: Toxicology Authors: Simin Zhao Yao Tan Jianning Qin Haiqiang Xu Lingyun Liu Hengquan Wan Chi Zhang Wenjing Fan Shunlin Qu Source Type: research
LINC01013 Is a Determinant of Fibroblast Activation and Encodes a Novel Fibroblast-Activating Micropeptide
AbstractMyocardial fibrosis confers an almost threefold mortality risk in heart disease. There are no prognostic therapies and novel therapeutic targets are needed. Many thousands of unannotated small open reading frames (smORFs) have been identified across the genome with potential to produce micropeptides (< 100 amino acids). We sought to investigate the role of smORFs in myocardial fibroblast activation.Analysis of human cardiac atrial fibroblasts (HCFs) stimulated with profibrotic TGF β1 using RNA sequencing (RNA-Seq) and ribosome profiling (Ribo-Seq) identified long intergenic non-coding RNA LINC01013 as TGFβ1...
Source: Journal of Cardiovascular Translational Research - June 27, 2022 Category: Cardiology Source Type: research
Salidroside attenuates myocardial ischemia/reperfusion injury via AMPK-induced suppression of endoplasmic reticulum stress and mitochondrial fission
In this study, we established a myocardial ischemia/reperfusion (I/R) rat model. Rat hearts exposed to Sal with or without compound C were then subjected to I/R. Further, H9c2 cardiomyocytes were subjected to simulated ischemia/reperfusion (SIR) by hypoxia-reoxygenation. The rats and cardiomyocytes were pretreated with Sal, followed by Compound C and AMPK-siRNA to block AMPK activity. We found that Sal significantly ameliorated cardiac function, mitigated infarct size and serum content of lactate dehydrogenase and creatine kinase, improved mitochondrial function, and reduced mitochondrial fission and apoptosis. Furthermore...
Source: Toxicology and Applied Pharmacology - June 6, 2022 Category: Toxicology Authors: Xin Tian Ye Huang Xiaofeng Zhang Rong Fang Yi Feng Wanfang Zhang Ling Li Tian Li Source Type: research
TMEM16A Plays an Insignificant Role in Myocardium Remodeling but May Promote Angiogenesis of Heart During Pressure-overload
Conclusion: TMEM16A contributes insignificantly in myocardium remodeling during pressure-overload. TMEM16A is a positive regulator of migration and angiogenesis under normal condition or simulated stress. TMEM16A may become a new target for upregulation of angiogenesis in ischemic disorders like ischemic heart disease.
Source: Frontiers in Physiology - May 31, 2022 Category: Physiology Source Type: research
SORBS2 as a molecular target for atherosclerosis in patients with familial hypercholesterolemia
CONCLUSIONS: SORBS2 regulates lipid-induced inflammation and foam cell formation, and is a potential therapeutic target for hypercholesterolemia.PMID:35590369 | DOI:10.1186/s12967-022-03381-z
Source: Atherosclerosis - May 19, 2022 Category: Cardiology Authors: Ming-Ming Liu Jia Peng Yuan-Lin Guo Cheng-Gang Zhu Na-Qiong Wu Rui-Xia Xu Qian Dong Chuan-Jue Cui Jian-Jun Li Source Type: research
Chaperone Mediated Autophagy Protects Cardiomyocytes Against Hypoxic-Cell Death
This study for the first time establishes a protective role for CMA (via Lamp2a overexpression) against hypoxia-induced cardiomyocyte loss and reveals the intriguing possibility that CMA activation may offer a cardioprotective treatment for ischemic heart disease.PMID:35584327 | DOI:10.1152/ajpcell.00369.2021
Source: Am J Physiol Cell Ph... - May 18, 2022 Category: Cytology Authors: Rajeshwary Ghosh Jennifer Jason Gillaspie Kenneth S Campbell J David Symons Sihem Boudina James Scott Pattison Source Type: research
