Mitofilin in cardiovascular diseases: Insights into the pathogenesis and potential pharmacological interventions

Abstract

The impact of mitochondrial dysfunction on the pathogenesis of cardiovascular disease is increasing. However, the precise underlying mechanism remains unclear. Mitochondria produce cellular energy through oxidative phosphorylation while regulating calcium homeostasis, cellular respiration, and the production of biosynthetic chemicals. Nevertheless, problems related to cardiac energy metabolism, defective mitochondrial proteins, mitophagy, and structural changes in mitochondrial membranes can cause cardiovascular diseases via mitochondrial dysfunction. Mitofilin is a critical inner mitochondrial membrane protein that maintains cristae structure and facilitates protein transport while linking the inner mitochondrial membrane, outer mitochondrial membrane, and mitochondrial DNA transcription. Researchers believe that mitofilin may be a therapeutic target for treating cardiovascular diseases, particularly cardiac mitochondrial dysfunctions. In this review, we highlight current findings regarding the role of mitofilin in the pathogenesis of cardiovascular diseases and potential therapeutic compounds targeting mitofilin.

Keywords: Bendavia (elamipretide) (PubChem CID: 11764719); Cardiovascular diseases; Cristae junction; Ginsenoside Rg1 (PubChem CID: 441923); Levosimendan (PubChem CID: 3033825); Malvidin 3-O-arabinoside (M3A) (PubChem CID: 91810654); Mito-tempo (PubChem CID: 134828258); MitoQ (PubChem CID: 11388332); Mitochondrial dysfunction; Mitochondrial-targeted therapy; Mitochonic Acid-5 (PubChem CID: 76070959); Mitofilin; N-acety-l-cysteine (PubChem CID: 12035); Pyridostatin (PubChem CID: 25227847); Resveratrol (PubChem CID: 445154).