Progranulin deficiency induces premature vascular senescence and dysfunction.

Renata de Azevedo Melo Luvizotto, André F Nascimento, Gustavo F Pimenta, Rafael M de Costa, Tyler Beling, Shubhnita Singh, Juliano V Alves, Wanessa M C Awata, Angela Russ, Adeyeye Isaac Haastrup, Rolando A Cuevas, Parya Behzadi, Cynthia St Hilaire, Justin T Roberts, Ariane Bruder, Thiago Bruder-Nascimento

Department of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama, United States.Department of Physiology and Cell Biology, University of South Alabama, Mobile, Alabama, United States. · pubmed

Paper

Abstract

Cellular senescence-an age-associated state characterized by irreversible cell cycle arrest and proinflammatory signaling-contributes to vascular dysfunction and cardiovascular disease. However, the molecular mechanisms linking senescence to vascular impairment remain incompletely defined. Progranulin (PGRN) is a multifunctional protein involved in inflammation, lysosomal function, and cellular homeostasis, but its role in vascular aging is not well understood. We assessed PGRN expression in human and mouse arteries and in senescent vascular smooth muscle cells (VSMCs). Vascular function was examined in PGRN-deficient (

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Research summary

Progranulin deficiency accelerates vascular aging and dysfunction by inducing premature senescence in vascular smooth muscle cells. This study identifies a specific molecular mechanism linking a known protein to age-related vascular decline, offering a potential target for interventions but representing an incremental step in understanding senescence rather than a transformative breakthrough in lifespan extension.

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