TMBIM-2 links neuronal mitochondrial stress to systemic adaptation via calcium signaling.

Yu Sun, Terytty Yang Li

State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Laboratory of Longevity and Metabolic Adaptations, Institute of Metabolism and Integrative Biology, Fudan University , Shanghai, China.State Key Laboratory of Genetic Engineering, Shanghai Key Laboratory of Metabolic Remodeling and Health, Laboratory of Longevity and Metabolic Adaptations, Institute of Metabolism and Integrative Biology, Fudan University , Shanghai, China. · pubmed

Paper

Abstract

Mitochondrial function is critical for neuronal activity and systemic metabolic adaptation. In this issue, Li et al. (https://doi.org/10.1083/jcb.202408050) identify TMBIM-2 as a key regulator of calcium dynamics, coordinating the neuronal-to-intestinal mitochondrial unfolded protein response (UPRmt), pathogen-induced aversive learning, and aging.

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Research summary

TMBIM-2 regulates calcium dynamics to coordinate mitochondrial stress responses that influence aging and systemic adaptation. The paper addresses mitochondrial function and its role in aging, linking cellular stress responses to broader systemic effects, which is pertinent to understanding the mechanisms of aging.

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