ArticleJournal of cellular and molecular medicine2020
FABP4 inhibitor BMS309403 protects against hypoxia-induced H9c2 cardiomyocyte apoptosis through attenuating endoplasmic reticulum stress.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- SMURF2-Mediated Ubiquitination and Degradation of HOXA5 Augments Endoplasmic Reticulum Stress in Alveolar Epithelial Type II Cells Induced by LPS.Molecular biotechnology · 2026Article
- FABP4 as an immunometabolic hub in preeclampsia: from maternal-fetal interface to systemic inflammation.Frontiers in immunology · 2026Review
- A novel high-throughput screening platform to identify inhibitors of DNAJB1-PRKACA-driven transcriptional activity in fibrolamellar carcinoma.SLAS discovery : advancing life sciences R & D · 2025Article
- The role of hydrogen sulfide in the regulation of necroptosis across various pathological processes.Molecular and cellular biochemistry · 2025Review
- Research progress of hypoxia-inducible factor-1α and zinc in the mechanism of diabetic kidney disease.Frontiers in pharmacology · 2025Review
- Article
- The Role of Epicardial Adipose Tissue in Acute Coronary Syndromes, Post-Infarct Remodeling and Cardiac Regeneration.International journal of molecular sciences · 2024Review
- FABP4 mediates endoplasmic reticulum stress and autophagy to regulate endometrial epithelial cell function during early sheep gestation.The Journal of reproduction and development · 2023Article
- Article
- Endoplasmic reticulum homeostasis: a potential target for diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Interleukin-4-induced FABP4 promotes lipogenesis in human skeletal muscle cells by activating the PPAR γ signaling pathway.Cell biochemistry and biophysics · 2022Article
- Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis.Cell death & disease · 2022Article
- Interaction between COX-2 and ER stress is involved in the apoptosis-induced myocardial ischemia/reperfusion injury.American journal of translational research · 2022Article
- Single-cell RNA sequencing analysis to characterize cells and gene expression landscapes in atrial septal defect.Journal of cellular and molecular medicine · 2021Article
- FABP4 inhibitor BMS309403 protects against hypoxia-induced H9c2 cardiomyocyte apoptosis through attenuating endoplasmic reticulum stress.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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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
Acute myocardial infarction is characterized by ischaemia-induced cardiomyocyte apoptosis, in which the endoplasmic reticulum (ER) stress plays an important role. The fatty acid-binding protein-4 (FABP4) has been implicated in regulating ER stress and apoptosis. Yet, whether FABP4 is involved in modulating cardiomyocyte apoptosis remains unclarified. By applying an in vitro model of hypoxia-induced apoptosis of H9c2 cardiomyocytes, we found that FABP4 expression was elevated upon hypoxia stimulation, which was further demonstrated to be transcriptionally activated by the hypoxia-inducible factor 1a (HIF-1α). In addition, the pharmacological inhibition of FABP4 with BMS309403 protected against hypoxia-induced apoptosis in cardiomyocytes, indicating that FABP4 induction is detrimental for cardiomyocyte survival under hypoxic condition. Moreover, BMS309403 attenuated ER stress in cardiomyocytes exposed to hypoxia, which, however, was reversed by tunicamycin, an ER stress activator. More importantly, the protective effect of BMS309403 on cardiomyocytes vanished in the presence of tunicamycin. Thus, these observations establish that FABP4 inhibitor BMS309403 reduces hypoxia-induced cardiomyocyte apoptosis through attenuating excessive ER stress, implying that FABP4 inhibition may be of clinical benefit for MI treatment.
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