ArticleApoptosis : an international journal on programmed cell death2022
MicroRNA-136-5p protects cardiomyocytes from coronary microembolization through the inhibition of pyroptosis.
Article in Apoptosis : an international journal on programmed cell death, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Expression of urinary exosomal miR-136-5p in diabetic kidney disease and evaluation of its clinical diagnostic value.Scientific reports · 2025Article
- Article
- Research Progress of Regulatory Cell Death in Coronary Microembolization.International journal of medical sciences · 2025Review
- Molecular Mechanisms and Roles of MiR-136-5p in Human Cancer and Other Disorders.Current medicinal chemistry · 2025Review
- Rising impact of cell death research.Apoptosis : an international journal on programmed cell death · 2023Article
- Functional implications of paralog genes in polyglutamine spinocerebellar ataxias.Human genetics · 2023Review
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
This study investigated how miR-136-5p partially affected cardiomyocyte pyroptosis in rats with coronary microembolization (CME). The cardiac function and structure of rats with CME were evaluated using echocardiography, hematoxylin and eosin staining, Masson staining, and troponin I level. Pyroptosis was induced by lipopolysaccharide (LPS) in isolated rat cardiomyocytes and evaluated by the expression of caspase-1, NOD-like receptor family pyrin domain-containing 3, interleukin-1β, and gasdermin D-N. After cell transfection, the expression of Ataxin-1 like (ATXN1L), pyrin domain-containing 1 (PYDC1), and pyroptosis-related proteins was assessed. Dual-luciferase reporter and immunoprecipitation assays were used to verify the relationships among miR-136-5p, ATXN1L, and capicua (CIC). MiR-136-5p was under-expressed, whereas ATXN1L was overexpressed in rats with CME and in LPS-treated primary cardiomyocytes. MiR-136-5p targeted ATXN1L, and ATXN1L bound to CIC to suppress PYDC1 expression. MiR-136-5p overexpression suppressed pyroptosis by inhibiting the binding of ATXN1L with CIC and promoting PYDC1 expression, which was reversed by simultaneous elevation of ATXN1L. In conclusion, miR-136-5p suppressed pyroptosis by upregulating PYDC1 via ATXN1L/CIC axis, thereby attenuating cardiac damage caused by CME.
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