Mitochondrial Permeability Transition Regulators As Emerging Therapeutic Targets in Aging and Neurodegeneration: Recent Insights.

Lishu Guo

Vagelos College of Physicians and Surgeons, Columbia University, New York, USA. [email protected] College of Physicians and Surgeons, Columbia University, New York, USA. [email protected]. · pubmed

Paper

Abstract

Aging is characterized by increased reactive oxygen species (ROS) and leads to mitochondrial dysfunction. This age-related decline in mitochondrial function is a major factor in the development of neurodegenerative diseases. Mitochondrial permeability transition pore (PTP) is a multi-protein complex that forms a non-specific channel across the inner mitochondrial membrane, and its opening is tightly linked to mitochondrial function and cell death. Dysregulation of PTP opening is now recognized as a central pathogenic mechanism in both normal aging and age-associated neurodegenerative diseases. This review integrates current understanding of mitochondrial permeability transition with emerging evidence implicating three novel regulatory components: F-ATP synthase inhibitory factor 1 (IF1), subunit j of F-ATP synthase, and mitochondrial carrier homolog 2 (MTCH2), expanding the therapeutic landscape for treating aging and neurodegeneration through targeting the PTP.

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Research summary

This review proposes that targeting specific regulatory components of the mitochondrial permeability transition pore (IF1, subunit j, MTCH2) may mitigate mitochondrial dysfunction and cell death associated with aging and neurodegeneration. The paper is relevant because it addresses mitochondrial dysfunction, a fundamental hallmark of aging, by discussing potential therapeutic interventions for age-related decline rather than merely treating symptoms of specific diseases.

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