The DOI matches its Crossref record; 149 of the 149 references it cites were found in a registry or an index.
Molecular mechanisms of renal aging
Open accessAbstract
Epidemiologic, clinical, and molecular evidence suggest that aging is a major contributor to the increasing incidence of acute kidney injury and chronic kidney disease. The aging kidney undergoes complex changes that predispose to renal pathology. The underlying molecular mechanisms could be the target of therapeutic strategies in the future. Here, we summarize recent insight into cellular and molecular processes that have been shown to contribute to the renal aging phenotype.The main clinical finding of renal aging is the decrease in glomerular filtration rate, and its structural correlate is the loss of functioning nephrons. Mechanistically, this has been linked to different processes, such as podocyte hypertrophy, glomerulosclerosis, tubular atrophy, and gradual microvascular rarefaction. Renal functional recovery after an episode of acute kidney injury is significantly worse in elderly patients. This decreased regenerative potential, which is a hallmark of the aging process, may be caused by cellular senescence. Accumulation of senescent cells could explain insufficient repair and functional loss, a view that has been strengthened by recent studies showing that removal of senescent cells results in attenuation of renal aging. Other potential mechanisms are alterations in autophagy as an important component of a disturbed renal stress response and functional differences in the inflammatory system. Promising therapeutic measures to counteract these age-related problems include mimetics of caloric restriction, pharmacologic renin-angiotensin-aldosterone system inhibition, and novel strategies of senotherapy with the goal of reducing the number of senescent cells to decrease aging-related disease in the kidney.
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“As individuals age, the kidneys undergo various structural impairments, such as fibrosis, and experience functional issues, including mitochondrial dysfunction (Fig. 3).144–146”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [146]
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Metadata
- Authors
- Schmitt, R., & Melk, A.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2017-09
- Volume
- 92
- Issue
- 3
- Pages
- 569-579
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2737090018
- Cited by
- 235
- References
- 149
- Citations by year
- 2026: 18 · 2025: 27 · 2024: 31 · 2023: 32 · 2022: 30 · 2021: 32 · 2020: 29 · 2019: 19 · 2018: 15 · 2017: 2
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Kidney International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Keywords
- kidney aging, acute kidney injury, chronic kidney disease, glomerular filtration rate decline, nephron loss, podocyte hypertrophy, glomerulosclerosis, tubular atrophy, microvascular rarefaction, cellular senescence, senolytics, autophagy, renal inflammation, caloric restriction mimetics, renin-angiotensin-aldosterone system inhibition, kidney regeneration
- MeSH terms
- Aging, Angiotensin-Converting Enzyme Inhibitors, Animals, Autophagy, Disease Models, Animal, Disease Susceptibility, Glomerular Filtration Rate, Humans, Kidney, Renin-Angiotensin System, Cellular Senescence, Caloric Restriction, Acute Kidney Injury
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