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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

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

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

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