ArticleThe Kaohsiung journal of medical sciences2023
CircHECTD1 promoted MIRI-associated inflammation via inhibiting miR-138-5p and upregulating ROCK2.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- miR-138-5p Promotes HF in Rats by Reducing Histone Methylation in the Myd88 Promoter Region through Inhibition of EZH2.Acta Cardiologica Sinica · 2026Article
- Guanxinjing ameliorates coronary microvascular dysfunction in myocardial ischemia-reperfusion injury by alleviating inflammation and restoring endothelial function.Frontiers in immunology · 2026Article
- Bone marrow mesenchymal stem cell-derived circHECTD1 targets claudin1 through the CTCF/METTL3 axis to alleviate ulcerative colitis : Short title: BMSC-derived circHECTD1 alleviates UC.Cellular and molecular life sciences : CMLS · 2025Article
- Indobufen alleviates apoptosis by the PI3K/Akt/eNOS pathway in myocardial ischemia‒reperfusion (I/R) injury.Scientific reports · 2025Article
- Shen-fu Injection Modulates HIF- 1α/BNIP3-Mediated Mitophagy to Alleviate Myocardial Ischemia-Reperfusion Injury.Cardiovascular toxicology · 2025Article
- CircRNA Networks in CAD: Multi-Cellular Mechanisms and Clinical Potential.International journal of general medicine · 2025Review
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- The emerging roles of circHECTD1 in human diseases and the specific underlying regulatory mechanisms.PeerJ · 2024Review
- CircHECTD1 promoted MIRI-associated inflammation via inhibiting miR-138-5p and upregulating ROCK2.The Kaohsiung journal of medical sciences · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia-reperfusion injury (MIRI) was often observed after surgeries, causing a lot of suffering to patients. Inflammation and apoptosis were critical determinants during MIRI. We conveyed experiments to reveal the regulatory functions of circHECTD1 in MIRI development. The Rat MIRI model was established and determined by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. We analyzed cell apoptosis using TUNEL and flow cytometry. Proteins expression was evaluated by western blot. The RNA level was determined by qRT-PCR. Secreted inflammatory factors were analyzed by ELISA assay. To predict the interaction sequences on circHECTD1, miR-138-5p, and ROCK2, bioinformatics analysis was performed. Dual-luciferase assay was used to confirm these interaction sequences. CircHECTD1 and ROCK2 were upregulated in the rat MIRI model, while miR-138-5p was decreased. CircHECTD1 knockdown alleviated H/R-induced inflammation in H9c2 cells. Direct interaction and regulation of circHECTD1/miR-138-5p and miR-138-5p/ROCK2 were confirmed by dual-luciferase assay. CircHECTD1 promoted H/R-induced inflammation and cell apoptosis by inhibiting miR-138-5p. miR-138-5p alleviated H/R-induced inflammation, while ectopic ROCK2 antagonized such effect of miR-138-5p. Our research suggested that the circHECTD1-modulated miR-138-5p suppressing is responsible for ROCK2 activation during H/R-induced inflammatory response, providing a novel insight into MIRI-associated inflammation.
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