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GZMK Drives Aging-Associated Fibrosis through Complement C3a/C3aR-Dependent Cellular Senescence

2025-11-13

Abstract excerpt

<title>Abstract</title> <p>Background Aging-related multi-organ fibrosis represents a major clinical challenge, largely due to poorly defined extracellular triggers of cellular senescence and the senescence-associated secretory phenotype (SASP). Granzyme K (GZMK), an immune cell–derived serine protease, is hypothesized to regulate this process through a previously unreported immunoproteolytic cascade. Given the e...

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Literature Corpus work
54d97359-1cfd-5d51-9d7d-84ad7a2dc257
DOI
10.21203/rs.3.rs-7888848/v1
Open publication

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GZMK Drives Aging-Associated Fibrosis through Complement C3a/C3aR-Dependent Cellular SenescenceDOI 10.21203/rs.3.rs-7888848/v1
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