ArticleThe Journal of clinical investigation2022
Age-related GSK3β overexpression drives podocyte senescence and glomerular aging.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 89 citations in OpenAlex.
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- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Gut microbiota modulates synaptic plasticity, connectivity, and dopamine transmission in the VTA-mPFC pathway in bipolar depression.Molecular psychiatry · 2026Article
- Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026Review
- From a Shared Stress to Cell-Type-Specific Responses: The Heterogeneous Mechanisms of High Glucose-Induced Cellular Senescence in Diabetic Kidney Disease.Journal of diabetes research · 2026Review
- circHERC1-A telomerase activator.Science advances · 2025Article
- Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025Review
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Decoy Receptor 2 as a Cell Cycle Arrest Biomarker for Predicting Renal Recovery Following Acute Kidney Injury.Journal of cellular and molecular medicine · 2025Article
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- Dapagliflozin, in addition to ramipril, ameliorates kidney disease progression in mice with Alport syndrome.American journal of physiology. Renal physiology · 2025Article
- Loss of Nup155 promotes high fructose-driven podocyte senescence by inhibiting INO80 mRNA nuclear export.Journal of advanced research · 2025Article
- Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage.JCI insight · 2025Article
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- Aging-dependent YAP1 reduction contributes to AD pathology by upregulating the Nr4a1-AKT/GSK-3β axis.Translational neurodegeneration · 2025Article
- NAT10 mediates TLR2 to promote podocyte senescence in adriamycin-induced nephropathy.Cell death & disease · 2025Article
- Uncovering Overlapping Gene Networks and Potential Therapeutic Targets in Osteoporosis and COVID-19 Through Bioinformatics Analysis.International journal of endocrinology · 2025Article
- SGLT2 inhibition attenuates diabetic tubulopathy by suppressing SGK1-mediated pyroptosis.Frontiers in endocrinology · 2025Article
Corrections and comments
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- Erratum issued
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
As life expectancy continues to increase, clinicians are challenged by age-related renal impairment that involves podocyte senescence and glomerulosclerosis. There is now compelling evidence that lithium has a potent antiaging activity that ameliorates brain aging and increases longevity in Drosophila and Caenorhabditis elegans. As the major molecular target of lithium action and a multitasking protein kinase recently implicated in a variety of renal diseases, glycogen synthase kinase 3β (GSK3β) is overexpressed and hyperactive with age in glomerular podocytes, correlating with functional and histological signs of kidney aging. Moreover, podocyte-specific ablation of GSK3β substantially attenuated podocyte senescence and glomerular aging in mice. Mechanistically, key mediators of senescence signaling, such as p16INK4A and p53, contain high numbers of GSK3β consensus motifs, physically interact with GSK3β, and act as its putative substrates. In addition, therapeutic targeting of GSK3β by microdose lithium later in life reduced senescence signaling and delayed kidney aging in mice. Furthermore, in psychiatric patients, lithium carbonate therapy inhibited GSK3β activity and mitigated senescence signaling in urinary exfoliated podocytes and was associated with preservation of kidney function. Thus, GSK3β appears to play a key role in podocyte senescence by modulating senescence signaling and may be an actionable senostatic target to delay kidney aging.
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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.