Podocyte injury at young age causes premature senescence and worsens glomerular aging

Author:

Veloso Pereira Beatriz Maria12,Zeng Yuting3ORCID,Maggiore Joseph C.4ORCID,Schweickart Robert Allen5ORCID,Eng Diana G.1ORCID,Kaverina Natalya1ORCID,McKinzie Sierra R.1,Chang Anthony6ORCID,Loretz Carol J.1,Thieme Karina2ORCID,Hukriede Neil A.4,Pippin Jeffrey W.1ORCID,Wessely Oliver5ORCID,Shankland Stuart J.17ORCID

Affiliation:

1. Division of Nephrology, University of Washington, Seattle, Washington, United States

2. Department of Physiology and Biophysics, University of São Paulo, São Paulo, Brazil

3. Department of Chemistry, University of Washington, Seattle, Washington, United States

4. Department of Developmental Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States

5. Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, United States

6. Department of Pathology, University of Chicago, Chicago, Illinois, United States

7. Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, United States

Abstract

Glomerular function is decreased by aging. However, little is known about the molecular mechanisms involved in age-related glomerular changes and which factors could contribute to a worse glomerular aging process. Here, we reported that podocyte injury in young mice and culture podocytes induced senescence, a marker of aging, and accelerates glomerular aging when compared with healthy aging mice.

Funder

Fundação de Amparo à Pesquisa do Estado de São Paulo

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

U.S. Department of Defense

University of Pittsburgh

Publisher

American Physiological Society

Subject

Physiology

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Injury in nonaged podocytes as an accelerator of glomerular aging;American Journal of Physiology-Renal Physiology;2024-01-01

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