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Review
. 2025 Sep 8.
doi: 10.1007/s11427-024-3037-1. Online ahead of print.

Mitochondria-lysosome crosstalk in microbial infections

Qianqian He  1 , Tiantian Huang  1 , Zhihui Chen  1 , Zhou Sha  1 , Haibo Wu  2
Affiliations
Review

Mitochondria-lysosome crosstalk in microbial infections

Qianqian He et al. Sci China Life Sci. .

Abstract

Coordination between different organelles and metabolic cues is crucial for resistance to pathogen invasion. As the core of maintaining cellular metabolism and homeostasis, mitochondria and lysosomes cooperate in the immune responses and elimination of intracellular pathogens. Previous research has focused on the function of one or the other in isolation, ignoring their pervasive interplay. In this review, we discuss the intricate mechanism of mitochondria-lysosome crosstalk and point out the role of AMP-activated protein kinase (AMPK)-transcription factor EB (TFEB) axis in microbial infections. The crosstalk between mitochondria and lysosomes affects cellular key processes, such as autophagy and programmed death, which play an important role in microbial infections.

Keywords: MDVs; lysosomes; microbial infections; mitochondria; mitophagy.

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Conflict of interest statement

Compliance and ethics. The authors declare that they have no conflict of interest.

References

    1. Abuaita, B.H., Schultz, T.L., and O’Riordan, M.X. (2018). Mitochondria-derived vesicles deliver antimicrobial reactive oxygen species to control phagosome-localized Staphylococcus aureus. Cell Host Microbe 24, 625–636.e5. - PubMed - PMC - DOI
    1. Ahola, S., Rivera Mejiás, P., Hermans, S., Chandragiri, S., Giavalisco, P., Nolte, H., and Langer, T. (2022). OMA1-mediated integrated stress response protects against ferroptosis in mitochondrial cardiomyopathy. Cell Metab 34, 1875–1891.e7. - PubMed - DOI
    1. Alix, E., Mukherjee, S., and Roy, C.R. (2011). Subversion of membrane transport pathways by vacuolar pathogens. J Cell Biol 195, 943–952. - PubMed - PMC - DOI
    1. Ammanathan, V., Mishra, P., Chavalmane, A.K., Muthusamy, S., Jadhav, V., Siddamadappa, C., and Manjithaya, R. (2020). Restriction of intracellular Salmonella replication by restoring TFEB-mediated xenophagy. Autophagy 16, 1584–1597. - PubMed - DOI
    1. Baixauli, F., Acín-Pérez, R., Villarroya-Beltrí, C., Mazzeo, C., Nuñez-Andrade, N., Gabandé-Rodriguez, E., Ledesma, M.D., Blázquez, A., Martin, M.A., Falcón-Pérez, J. M., et al. (2015). Mitochondrial respiration controls lysosomal function during inflammatory T cell responses. Cell Metab 22, 485–498. - PubMed - PMC - DOI

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