Regulation of mitochondria functions by Mycobacterium tuberculosis infection

Tuberculosis, a leading killer among infectious diseases worldwide, is caused by Mycobacterium tuberculosis (Mtb). Mtb has strong ability to manipulate the intracellular environment of macrophages for successful surviving. Mitochondrion is a key organelle involved in diverse physiological processes, including Ca²⁺ fluxes, ATP synthesis, bioenergetic metabolism, and cell death, which are pivotal to cellular and organismal homeostasis. Mitochondrion is also targeted by Mtb to control various physiological responses of the host. Mtb has evolved a series of strategies to manipulate mitochondrial functions in favor of their survival, replication, and dissemination. In mitochondrion, Mtb regulates cell energy metabolism and cell death pathway. Herein, we reviewed the latest advances in the interactions between Mtb and mitochondria and discussed multiple aspects of the influence of Mtb on mitochondrial metabolism to shed light on the Mtb-induced pathogenesis.