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RESEARCH PAPER / 2026-10-13

CHCHD2 mitigates age-associated proteostatic collapse by maintaining homeostasis of the mitochondria-lysosome axis.

Teresa R Kee, Brianna M Masters, Khoi D Tran, Hanna Jeon, Ma Long, Grace Xu, Sophia A Khan, Edwin Vázquez-Rosa, Preethy S Sridharan, Yeojung Koh, Hisashi Fujioka, Dale Chaput, Xinming Wang, Xingyu Zhao, Andrew A Pieper, David E Kang, Jung-A A Woo

Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH, USA. · pubmed

Abstract

Mutations in coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2), including the Parkinson's disease (PD)-linked CHCHD2

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

CHCHD2 mutations cause age-associated proteostatic collapse by disrupting the mitochondria-lysosome axis, and maintaining this homeostasis mitigates the resulting cellular dysfunction. This paper is relevant because it identifies a specific molecular mechanism (the mitochondria-lysosome axis) underlying proteostatic failure, a core hallmark of aging, and links it to a known genetic risk factor for neurodegeneration, offering a potential target for interventions aimed at preserving cellular health during aging.

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