FABP4 inhibitor BMS309403 protects against hypoxia‐induced H9c2 cardiomyocyte apoptosis through attenuating endoplasmic reticulum stress

Abstract

Acute myocardial infarction (MI), one of the leading causes of disability and death in the world, 1 is featured by the ischaemia-induced cardiomyocyte loss due to necrosis and apoptosis. 2 To date, increasing evidence has shown that the cardiomyocyte apoptosis spotted in the border zone of infarct lesions and the remote zone of non-infarcted myocardium deteriorates the post-MI remodelling and cardiac dysfunction, together contributing to heart failure development. 3,4 Therefore, advancing the mechanisms of cardiomyocyte apoptosis during the early stage of MI is extremely important for reversing this pathogenic process and ameliorating cardiac function of patients with MI.

Single‐cell RNA sequencing analysis to characterize cells and gene expression landscapes in atrial septal defect

“…Sun et al showed that inhibition of FABP4 could protect cardiomyocytes from apoptosis caused by hypoxia. 47 These genes were all differentially expressed in ASD and normal samples in this study. Similarly, in‐vitro assays have shown that Nppa participates in the regulation of cardiomyocyte apoptosis, with the altered expression of FABP4 and FOS.…”

Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis

“…Fatty acid-binding protein 4 (FABP4) is well known for its pathogenic effect in metabolic diseases such as atherosclerosis and diabetes mellitus [ 19 – 21 ]. Recently, FABP4 has also emerged as a critical player in inflammation and apoptosis in various pathological processes [ 22 – 24 ]. We previously found that FABP4 expression increased in injured RTECs of ischemia/reperfusion-, rhabdomyolysis-, and cisplatin-induced AKI, and FABP4 inhibition by BMS309403 alleviated tubular injury, while the mechanisms of FABP4 upregulation were poorly understood [ 25 – 27 ].…”

Application of silver nanoparticles for improving motor recovery after spinal cord injury via reduction of pro-inflammatory M1 macrophages

“…Upregulated genes ( Fabp4, Col15a1, Cxcl14 and Slc8a1 ) associated to cell apoptosis were detected in M1. These upregulated DEGs implied AgNPs triggered apoptosis in M1 [ [32] , [33] , [34] , [35] ]. Moreover, we also observed that AgNPs resulted in 211 upregulated DEGs and 60 downregulated DEGs in M0, as well as 219 upregulated DEGs and 63 downregulated DEGs in M2 ( Fig.…”