ArticleAging2023
Inhibiting NLRP3 signaling in aging podocytes improves their life- and health-span.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- TXNIP-Deficiency and Prdx6 Delivery Inhibit Aging/Oxidative Stress-Driven TXNIP-Nlrp3 Inflammasome Activation and Mitigate Pyroptosis in Lens Epithelial Cells.Antioxidants (Basel, Switzerland) · 2026Article
- New potential therapeutic targets of metabolic disorder-associated kidney disease and diabetic kidney disease.Kidney international · 2026Review
- Inhibition of caspase-1 by ginsenoside Rg1 ameliorates d-gal-induced renal aging and injury through suppression of oxidative stress and inflammation.Renal failure · 2025Article
- Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Isolation of Podocyte Cell Fractions From Mouse Kidney Using Magnetic Activated Cell Sorting (MACS).Bio-protocol · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.Journal of the American Society of Nephrology : JASN · 2025Review
- Mechanism of activation of TLR4/NF-κB/NLRP3 signaling pathway induced by heat stress disrupting the filtration barrier in broiler.BMC veterinary research · 2024Article
- Podocyte senescence: from molecular mechanisms to therapeutics.Renal failure · 2024Review
- Pathological mechanisms of kidney disease in ageing.Nature reviews. Nephrology · 2024Review
- Podocytes from hypertensive and obese mice acquire an inflammatory, senescent, and aged phenotype.American journal of physiology. Renal physiology · 2024Article
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- Podocyte injury at young age causes premature senescence and worsens glomerular aging.American journal of physiology. Renal physiology · 2024Article
- Molecular Mechanisms Associated with Aging Kidneys and Future Perspectives.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
Abstract
The decrease in the podocyte's lifespan and health-span that typify healthy kidney aging cause a decrease in their normal structure, physiology and function. The ability to halt and even reverse these changes becomes clinically relevant when disease is superimposed on an aged kidney. RNA-sequencing of podocytes from middle-aged mice showed an inflammatory phenotype with increases in the NLRP3 inflammasome, signaling for IL2/Stat5, IL6 and TNF, interferon gamma response, allograft rejection and complement, consistent with inflammaging. Furthermore, injury-induced NLRP3 signaling in podocytes was further augmented in aged mice compared to young ones. The NLRP3 inflammasome (NLRP3, Caspase-1, IL1β IL-18) was also increased in podocytes of middle-aged humans. Higher transcript expression for NLRP3 in human glomeruli was accompanied by reduced podocyte density and increased global glomerulosclerosis and glomerular volume. Pharmacological inhibition of NLRP3 with MCC950, or gene deletion, reduced podocyte senescence and the genes typifying aging in middle-aged mice, which was accompanied by an improved podocyte lifespan and health-span. Moreover, modeling the injury-dependent increase in NLRP3 signaling in human kidney organoids confirmed the anti-senescence effect of MC9950. Finally, NLRP3 also impacted liver aging. Together, these results suggest a critical role for the NLRP3 inflammasome in podocyte and liver aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.