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RESEARCH PAPER / 2026-11-12

Granzyme K is a driver of age-related tissue remodeling and functional decline independently of age-associated immune dysfunction.

Dulakara Kannangara, Jessica Runting, April L Raftery, Ekaterina Salimova, Xavier Y X Sng, Ali Zaid, Samantha J Emery-Corbin, David Chisanga, Hui Xu, Angela Nguyen, Tania Camilleri, Joel A Eliades, Zijian Huang, Iona S Schuster, Ralf B Schittenhelm, Phillip I Bird, Laura Mackay, Kim L Good-Jacobson, Adam J Rose, Nicholas D Huntington, Mariapia Degli-Esposti, Christopher T Turner, Daniel Thiele, Nicole L La Gruta

Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. · pubmed

Abstract

Aging is characterized by progressive tissue and organ decline, with chronic low-grade inflammation (inflammaging) implicated as a central driver. Granzyme K (GzmK), a serine protease that is markedly upregulated in aged memory CD8

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

Granzyme K drives age-related tissue remodeling and functional decline independently of age-associated immune dysfunction. This paper identifies a specific molecular mechanism (GzmK) contributing to the physiological decline of aging, moving beyond general inflammation to pinpoint a driver of tissue damage, which is relevant to understanding the root causes of aging.

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