Aug 2026· Journal of biochemical and molecular toxicology· Vol 40 9, pp.
e70995
· 0 citations· 40 references
Medicine
TL;DR
It is demonstrated that the downregulation of circ_0001112 promoted cardiomyocyte apoptosis by sponging miR-324-5p and upregulating CDK6 expression in MI.
Abstract
Myocardial infarction (MI) usually results in severe heart failure (HF), and patients suffer from the repercussions of MI, elucidation of the pathological basis of MI is crucial to optimize the prevention and treatment of MI. This study investigated the role of dysregulated circ_0001112 in MI. In our study, circ_0001112 was significantly upregulated in the MI model and by hypoxia treatment. Circ_0001112 overexpression inhibited hypoxia-induced cardiomyocyte apoptosis. Luciferase assay showed that circ_0001112 sponged miR-324-5p that regulated the expression of cyclin-dependent kinase 6 (CDK6). Ago2-miRNP immunoprecipitation further confirmed that the 3'-untranslated region (3'UTR) of CDK6 was targeted by miR-324-5p. Either miR-324-5p overexpression or CDK6 knockdown prevented cardiomyocyte apoptosis induced by circ_0001112 overexpression. In conclusion, this study demonstrated that the downregulation of circ_0001112 promoted cardiomyocyte apoptosis by sponging miR-324-5p and upregulating CDK6 expression in MI.
The expression of the circRNA circKLHL20_009 was significantly upregulated in the myocardium of patients with heart failure and in human cardiomyocytes treated with angiotensin II and an artificial circRNA sponge, circSPmiR31, effectively mitigated cardiac hypertrophy and fibrosis by suppressing miR-31-5p binding to Dk...
Yi-hong Wen, Jia-xue Jiang, W. Dong et al.· Acta Pharmacologica Sinica· 0 citations
It is demonstrated that high glucose triggers regulator of G protein signaling 6 (RGS6) up-regulation in both human and murine cardiomyocytes, the hearts of hyperglycemic mice, and cardiac tissue samples from individuals with heart failure and a history of diabetes point to RGS6/KLF4 as key sources of pathogenic cardia...
Abhishek Singh Sengar, Sreemoyee Chakraborti, Anushree Lye et al.· Molecular and Cellular Endoc...· 0 citations
Cardiac aging is the major risk factor and important pathogenic foundation for cardiovascular diseases (CVDs) in the elderly. Various miRNAs have been reported to participate in this process. However, the precise mechanisms through which distinct miRNAs contribute to cardiac aging remain to be fully elucidated. In this...
Jun-Xi Liao, Chan Li, Min Zheng et al.· Tissue & Cell· 0 citations
MicroRNA-150-5p (miR-150) was correlated with heart failure (HF) severity in humans. Left ventricular homeobox a4 (HOXA4) was upregulated in patients with HF. Gain-of-function mutants in myocardial infarction-associated transcript (MIAT) were associated with increased risk of myocardial infarction (MI) in humans. O...
S. Kawaguchi, Marisa N. Sepúlveda, Taiki Hayasaka et al.· Cell Death & Disease· 0 citations
Summary Myocardial infarction (MI) remains the leading cause of death due to cardiovascular disease worldwide. role of MYZAP in angiogenesis remains unclear. The expression of MYZAP in MI was significantly decreased. Endothelial-specific overexpression of MYZAP improved cardiac function, increased angiogenesis, and res...
Li-Na Xuan, Guang-Ze Wang, Xiu-Fang Li et al.· iScience· 0 citations
Ventricular remodeling post-myocardial infarction (MI) is closely associated with immune responses; however, the underlying mechanisms remain incompletely understood. This study investigated whether the calcium-sensing receptor (CaSR) regulates macrophage (MΦ) polarization via the SIRT3-AMPK axis and its role in post-M...
Lin-Lin Song, Qi-Pei Liu, Nuo Chen et al.· International Immunopharmaco...· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
