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Succinate-specific effects are initiated by epigenetic alterations through the inhibition of KDMs and the TET family 5mC hydroxylases, which induce the translation of tumorigenic genes (Fig

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Computational models of complex Ca 2+ dynamics incorporating store-operated Ca 2+ entry and MAM geometry further underscore the nonlinear behavior of this system and its sensitivity to small changes in channel density, ER store content, or mitochondrial buffering capacity ( 2+ transfer and mitochondrial Ca 2+ overload are early pathogenic events, whereas oxidative stress, inflammatory activation, and impaired clearance of damaged mitochondria contribute mainly to propagation and amplification of acinar cell injury

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