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Cells
Volume 14
Issue 22
10.3390/cells14221831
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Review

From Senescent Cells to Systemic Inflammation: The Role of Inflammaging in Age-Related Diseases and Kidney Dysfunction

by
Federica De Luca
1,2,
Valentina Camporeale
1,2,
Giorgia Leccese
1,2,
Roberto Cuttano
1,2,
Dario Troise
2,3,
Barbara Infante
2,3,
Giovanni Stallone
2,3,
Giuseppe Stefano Netti
1,2,* and
Elena Ranieri
1,2
1
Unit of Clinical Pathology, Department of Medical and Surgical Sciences, University of Foggia—University Hospital “Policlinico Riuniti”, Viale Luigi Pinto, 71122 Foggia, Italy
2
Center for Research and Innovation in Medicine (CREATE), Department of Medical and Surgical Sciences, University of Foggia—University Hospital “Policlinico Riuniti”, Viale Luigi Pinto, 71122 Foggia, Italy
3
Unit of Nephrology, Dialysis and Transplantation, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia—University Hospital “Policlinico Riuniti”, Viale Luigi Pinto, 71122 Foggia, Italy
*
Author to whom correspondence should be addressed.
Cells 2025, 14(22), 1831; https://doi.org/10.3390/cells14221831
Submission received: 1 September 2025 / Revised: 11 November 2025 / Accepted: 17 November 2025 / Published: 20 November 2025
(This article belongs to the Special Issue The Role of Cellular Senescence in Health, Disease, and Aging)
Versions Notes

Abstract

Aging is characterized by a chronic, low-grade inflammatory state known as inflammaging, which closely interacts with immunosenescence—the gradual deterioration of immune function. Together, these processes contribute to tissue dysfunction and the development of age-related diseases. This review explores the cellular and molecular mechanisms underlying inflammaging, including mitochondrial dysfunction, telomere attrition, impaired autophagy, and gut microbiota dysbiosis. A particular emphasis is given to the senescence-associated secretory phenotype (SASP), which sustains a pro-inflammatory microenvironment and exacerbates tissue damage. We further discuss the impact of inflammaging on major age-related pathologies, with a focus on the kidney as a paradigmatic model of age-related decline, where inflammaging and cellular senescence contribute to chronic kidney disease (CKD) and impaired regeneration. Finally, we summarize emerging therapeutic strategies such as senolytics, senomorphics, immunomodulation, and lifestyle interventions, aimed at reducing the burden of senescent cells, mitigating inflammaging and extending healthspan.
Keywords: inflammaging; immunosenescence; cellular senescence; chronic kidney disease (CKD); senolytics inflammaging; immunosenescence; cellular senescence; chronic kidney disease (CKD); senolytics

Share and Cite

MDPI and ACS Style

Luca, F.D.; Camporeale, V.; Leccese, G.; Cuttano, R.; Troise, D.; Infante, B.; Stallone, G.; Netti, G.S.; Ranieri, E. From Senescent Cells to Systemic Inflammation: The Role of Inflammaging in Age-Related Diseases and Kidney Dysfunction. Cells 2025, 14, 1831. https://doi.org/10.3390/cells14221831

AMA Style

Luca FD, Camporeale V, Leccese G, Cuttano R, Troise D, Infante B, Stallone G, Netti GS, Ranieri E. From Senescent Cells to Systemic Inflammation: The Role of Inflammaging in Age-Related Diseases and Kidney Dysfunction. Cells. 2025; 14(22):1831. https://doi.org/10.3390/cells14221831

Chicago/Turabian Style

Luca, Federica De, Valentina Camporeale, Giorgia Leccese, Roberto Cuttano, Dario Troise, Barbara Infante, Giovanni Stallone, Giuseppe Stefano Netti, and Elena Ranieri. 2025. "From Senescent Cells to Systemic Inflammation: The Role of Inflammaging in Age-Related Diseases and Kidney Dysfunction" Cells 14, no. 22: 1831. https://doi.org/10.3390/cells14221831

APA Style

Luca, F. D., Camporeale, V., Leccese, G., Cuttano, R., Troise, D., Infante, B., Stallone, G., Netti, G. S., & Ranieri, E. (2025). From Senescent Cells to Systemic Inflammation: The Role of Inflammaging in Age-Related Diseases and Kidney Dysfunction. Cells, 14(22), 1831. https://doi.org/10.3390/cells14221831

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