ArticleCardiovascular diagnosis and therapy2022
TXNIP knockout improves cardiac function after myocardial infarction by promoting angiogenesis and reducing cardiomyocyte apoptosis.
Article in Cardiovascular diagnosis and therapy, 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.
- [Effects of exosomes derived from normoxic or hypoxic human umbilical vein endothelial cells on hypoxia-induced cardiomyocyte injury and cardiac fibroblast activationNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- TXNIP knockdown ameliorates hepatic ischemia/reperfusion injury by inhibiting apoptosis and improving mitochondrial dysfunction via HIF-1α.Molecular and cellular biochemistry · 2025Article
- Anti-angiogenesis and anti-immunosuppression gene therapy through targeting COUP-TFII in an in situ glioblastoma mouse model.Cancer gene therapy · 2024Article
- Blockade of thromboxane A2 signaling attenuates ethanol-induced myocardial inflammatory response in mice.Alcohol, clinical & experimental research · 2024Article
- TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.Acta biochimica et biophysica Sinica · 2023Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Myocardial Glutathione Synthase and TRXIP Expression Are Significantly Elevated in Hypertension and Diabetes: Influence of Stress on Antioxidant Pathways.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Myocardial infarction (MI) is a common cause of death. Thioredoxin-interacting protein (TXNIP) expression increases after MI, and it exerts a negative regulatory effect on cardiac function after MI. Our study aimed to investigate the specific regulatory mechanism of TXNIP on angiogenesis and cardiomyocyte apoptosis after MI. Methods: The Results: Compared with WT mice, Conclusions: After MI, TXNIP down-regulated the level of HIF-1α and VEGF, reduced the number of angiogenesis, increased cardiomyocyte apoptosis, and ultimately led to a poor prognosis of ischemic myocardium. TXNIP was a protein with negative effects after MI and was expected to be a target for the prevention and treatment of MI.
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