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Mitochondrial Ca2+ signaling: A metabolic rheostat defining tumor and immune cell fate
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DOI：10.1016/j.it.2026.05.012.png)
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Abstract
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Mitochondrial Ca2+ signaling functions as an immunometabolic control node that integrates tumor bioenergetics, redox balance, and stress adaptation with immune cell regulation. Dysregulated mitochondrial Ca2+ flux supports tumor metabolic flexibility and immune evasion while imposing bioenergetic and oxidative constraints that limit antitumor immune responses. Metabolic stress and Ca2+-dependent signaling pathways regulate immune checkpoint expression and antigen presentation, linking tumor metabolism directly to tumor antigenicity. Immune cells rely on finely tuned mitochondrial Ca2+ handling to sustain activation, migration, and effector functions, whereas chronic Ca2+ overload contributes to T cell exhaustion. Targeting mitochondrial Ca2+ dynamics offers a rational strategy to normalize the tumor microenvironment and overcome resistance to immune checkpoint blockade, which may represent next-generation combinatorial immunotherapies.
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