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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Apelin affects the mouse aging urinary peptidome with minimal effects on kidney
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Proteasome activator PA200 maintains stability of histone marks during transcription and agingPreprint
Jiang, T.-X., Ma, S., Han, X., Luo, Z.-Y., Zhu, Q., Chiba, T., Xie, W., Chen, S., Lin, K., & Qiu, X. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.04.28.067132 · Cited by 3
Keçeci, M., Özer, C. M., Babaoğlu, E., Bodur, F., Önal, A. C., Kayatekin, A. Z. Y., Cengil, O., & Karataş, A. S. (2025) · Scientific Reports · doi:10.1038/s41598-025-14559-y · Cited by 2
SGLT2 Inhibition Ameliorates Age-Dependent Renovascular Rarefaction
Paulmann, A., Cox, M. D., Boewer, T. J., Somers, H. M., Fuqua, J. H., Seaman, R. P., Graber, J. H., Mahajan, A., Johnson, C. P., Beverly-Staggs, L. L., et al. (2025) · Journal of the American Society of Nephrology · doi:10.1681/asn.2025aq07f04g · Cited by 3
Sodium-glucose co-transporter 2 inhibition improves age-dependent kidney microvascular rarefaction
Paulmann, A., Cox, M. D., Boewer, T. J., Somers, H. M., Fuqua, J. H., Seaman, R. P., Graber, J. H., Mahajan, A., Johnson, C. P., Beverly-Staggs, L. L., et al. (2025) · Kidney International · doi:10.1016/j.kint.2025.12.011 · Cited by 4
“2,20 Interestingly, we did not observe (global) glomerular hypertrophy during killifish aging: the mean diameter of glomeruli in aged kidneys stayed similar to that of young animals, but the overall distribution of various sizes increased significantly.”
Interleukin-6 in Natural and Pathophysiological Kidney Aging
Mutig, K., Singh, P. B., & Lebedeva, S. V. (2026) · Cells · doi:10.3390/cells15030225 · Cited by 2
“Accumulation of senescent cells in the aged kidney tissue is associated with enhanced local production of inflammatory cytokines [54,55].”
Febianti, Z., Permatasari, N., & Soeharto, S. (2019) · Asian Journal of Pharmaceutical and Clinical Research · doi:10.22159/ajpcr.2018.v12i1.29857 · Cited by 3
Chang, S.-C., Hsu, C., Liu, L.-K., Lu, Y., Tsai, Y.-L., Chou, R., Huang, P., Chen, L., & Lin, S. (2021) · Scientific Reports · doi:10.1038/s41598-021-99081-7 · Cited by 2
N1-Methylnicotinamide: The Mysterious Anti-aging Actor in Renal Transplantation
Nejabati, H. R., & Roshangar, L. (2023) · Current Pharmaceutical Design · doi:10.2174/1381612829666230330083649 · Cited by 3
Glomerular filtration rate and comorbidity factors in elderly hospitalizations
Hamarat, H. (2025) · World Journal of Nephrology · doi:10.5527/wjn.v14.i1.98837 · Cited by 2
Mecanismos de envejecimiento renal
Valverde, D. M., Brenes, I. A., & Muñoz, M. P. (2022) · Revista Medica Sinergia · doi:10.31434/rms.v7i5.804 · Cited by 2
The role of age and sex in non-linear dilution adjustment of spot urine arsenic
Carmine, T. C. (2024) · BMC Nephrology · doi:10.1186/s12882-024-03758-w · Cited by 2
“Hormonal factors additionally contribute to the gender difference in GFR decline as estrogens exert renoprotective effects by inhibiting the RAAS and facilitating advantages in methylation and antioxidation [10, 67, 68, 77, 78].”
Spécificité de la prise en charge du cancer du rein métastatique chez le patient âgé
Neuzillet, Y., Albrand, G., Caillet, P., Paillaud, É., & Mongiat-Artus, P. (2019) · The French Journal of Urology · doi:10.1016/j.purol.2019.08.272 · Cited by 2
Marunaka, Y., Yagi, K., Imagawa, N., Kobayashi, H., Murayama, M., Minamibata, A., Takanashi, Y., & Nakahari, T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222011111 · Cited by 2
“Abbreviations AE anion exchanger CA carbonic anhydrase CAI carbonic anhydrase I CAII carbonic anhydrase II CI confidence interval [Cl−]s venous serum Cl− concentration COPD chronic obstructive pulmonary disease DM diabetes mellitus FBS fasting blood sugar GFR glomerular filtration rate Hb hemoglobin HbA1c glycated hem…”
BackgroundInfluentialSarhan, N. R., Nashar, E. M. E., Hamza, E., El-Beah, S. M., Alghamdi, M. A., Al-Khater, K. M., Aldahhan, R. A., & Abul-Ela, E. S. A.-A. (2023) · Tissue and Cell · doi:10.1016/j.tice.2023.102192 · Cited by 2
Biomarkers for Chronic Kidney Disease: An Updated Review of Innovative Detection Approaches
Tolou–Ghamari, Z. (2025) · Current Aging Science · doi:10.2174/0118746098380113250707112707 · Cited by 2
Goki, M. M., Rostamzadeh, F., Jafarinejad‐Farsangi, S., Jafari, E., Soltani, Z., Mansouri, S., & Askarimoghadam, H. (2025) · European Journal of Applied Physiology · doi:10.1007/s00421-025-06005-8 · Cited by 1
Kwon, J. K., Kim, M., Lee, J., Oh, J.-I., Koh, J. H., Kang, M. W., Cho, J. H., Kim, S. G., Huh, H., Jung, S., et al. (2026) · Kidney International Reports · doi:10.1016/j.ekir.2026.106414 · Cited by 1
“34 Interestingly, the result of this study showed reversed pattern from conventional expectations such as hypertension, albuminuria, and smoking are risk factors for kidney failure.”
FOXP1 deficiency exacerbates cellular senescence in PM2.5-induced renal injury
Chen, H. X., Zhan, Z., Lü, M., Li, D., Peng, J., Chen, L., Yi, B., & Huang, Z. (2026) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2026.120071 · Cited by 1
Ketone bodies in kidney diseases: novel insights
Dai, W., Zhang, W., Li, H., Gao, Y., Xiao, L., Chen, Y., & He, L. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1738916 · Cited by 1
“…the core pathological foundations of kidney diseases, particularly in DN. Excessive accumulation of reactive oxygen species (ROS) triggers DNA damage, lipid peroxidation and mitochondrial dysfunction, thereby driving renal tubular epithelial cell apoptosis and interstitial in fl ammation (82, 83).”
Multi-omics profiling reveals systemic rejuvenation of the aged kidney through senolytic therapy
Chen, S., Zhang, C., Cang, P., Guo, W., Xiao, L., He, Y., Su, Q., Ouyang, S., Zha, J., Maimaitirexiati, G., et al. (2026) · npj Regenerative Medicine · doi:10.1038/s41536-026-00490-x · Cited by 1
“In the aging kidney, in fl ammatory mediators act not only as cell-intrinsic signals but also facilitate intercellular communication [31].”
Liu, N., & Liu, T. (2026) · International Urology and Nephrology · doi:10.1007/s11255-026-05271-5 · Cited by 1
Stress-induced senescence as a forme fruste of chronic kidney disease—A case for failed regeneration
Goligorsky, M. S. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823318-4.00001-9 · Cited by 1
Post-Trial Follow-Up of Kidney Outcomes in SPRINT
Ku, E., & Sarnak, M. J. (2024) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.0000000000000393 · Cited by 1
Implicaciones del proceso de envejecimiento renal en el adulto mayor
Sánchez, M. P. R., & Rey, R. D. (2024) · Medicina · doi:10.56050/01205498.2340 · Cited by 1
Age-Linked Non-Transmissible Diseases
Swynghedauw, B. (2019) · Practical issues in geriatrics · doi:10.1007/978-3-030-15111-9_6 · Cited by 1
Effects of a prolonged diet regimen on autophagic function in rat islets with aging
Gu, Z., Miao, X., Cui, J., Yang, F., Ma, L.-C., Li, C., Sun, B., & Yan, S. (2021) · Experimental Gerontology · doi:10.1016/j.exger.2021.111659 · Cited by 2
Pinto, S. W. L., Lima, H. D. N., Abreu, T. T. D., Otoni, A., Nogueira, P. C. K., & Sesso, R. (2022) · Kidney International Reports · doi:10.1016/j.ekir.2022.06.011 · Cited by 1
Reversal of the renal hyperglycemic memory by targeting sustained tubular p21 expressionPreprint
Al‐Dabet, M. M., Shahzad, K., Elwakiel, A., Sulaj, A., Kopf, S., Bock, F. M., Gadi, I., Zimmermann, S., Rana, R., Krishnan, S., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.07.05.450846 · Cited by 1
“expression causes tubular senescence and compromises tubular repair capacity in DKD patients (50), even after glycemic control has improved.”
BackgroundUpregulated PD-1 Signaling is an Important Antagonist to Glomerular Health in Aged KidneysPreprint
Pippin, J. W., Kaverina, N. V., Wang, Y., Eng, D. G., Zeng, Y., Tran, U., Loretz, C. J., Chang, A., O'Connor, C. L., Bitzer, M., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.10.26.466006 · Cited by 1
“As expected, staining for senescence-associated beta-galactosidase (SA-ßgal)(8) was higher in both glomeruli and tubular epithelial cells in aged mice (Figure 3B) when compared to their young counterparts (Figure 3A).”
BackgroundResultBolasco, P., Aquilani, R., Maestri, R., Esposito, M. P., Deiana, M. L., Cadeddu, M., Secci, R., Casu, B., Serra, A., Iadarola, P., et al. (2022) · Preprints.org · doi:10.20944/preprints202201.0371.v2 · Cited by 1
Hall, S., Brown, S. V., Amador, J. J., López-Pilarte, D., Ramírez‐Rubio, O., Sánchez, M. R. A., Gil, S. G., Argos, M., Carvalho, L. E., Henn, B. C., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5169119 · Cited by 1
Nankivell, B. J. (2019) · Elsevier eBooks · doi:10.1016/b978-0-323-53186-3.00027-9
Research Progress on the Relationship between Sirtuins and Renal Aging
赵, 舒. (2020) · Advances in Clinical Medicine · doi:10.12677/acm.2020.106171
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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