Mitophagy: A Potential Therapeutic Target for Tuberculosis Immunotherapy.

Abstract

Mitophagy serves as a cytoprotective mechanism that is essential for eliminating dysfunctional or superfluous mitochondria, thereby fine-tuning mitochondrial quantity and maintaining cellular homeostasis. Recent studies underscore the critical role of mitophagy in determining the fate and function of host cells infected by Mycobacterium tuberculosis. The successful pathogen strategically integrates into the host's mitochondrial network, manipulating processes such as apoptosis, metabolic reprogramming, mitochondrial fusion and fission, and reactive oxygen species production. Therefore, understanding those mechanisms is critical for the advancements of host-directed therapies against tuberculosis. This study offers a comprehensive overview of the interplay between Mycobacterium tuberculosis and mitophagy, emphasizing the associated signaling pathways and potential therapeutic targets involved in mitophagy in Mycobacterium tuberculosis infection. Activating mitophagy in infected host cells represents a promising avenue for improving therapeutic outcomes against tuberculosis. This review aims to summarize potential research direction for agents targeting induction of mitophagy. Notably, evidence suggests that BNIP3/NIX-mediated mitophagy may serve as a potential therapeutic target.