ArticleJournal of the American Society of Nephrology : JASN2015
Murine Double Minute-2 Prevents p53-Overactivation-Related Cell Death (Podoptosis) of Podocytes.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Diagnostic value of the correlation between urinary MDM2 and podocyte mitotic catastrophe in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- MicroRNAs at the crossroads of exercise and ferroptosis: a regulatory bridge.Clinical and experimental medicine · 2025Review
- The Impact of METTL3 on MDM2 Promotes Podocytes Injury During Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2025Article
- Cell cycle disorders in podocytes: an emerging and increasingly recognized phenomenon.Cell death discovery · 2025Review
- Hyperactivation of p53 contributes to mitotic catastrophe in podocytes through regulation of the Wee1/CDK1/cyclin B1 axis.Renal failure · 2024Article
- Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets.International journal of molecular sciences · 2024Review
- Cyclin-dependent kinase 7 (CDK7) inhibitors as a novel therapeutic strategy for different molecular types of breast cancer.British journal of cancer · 2024Review
- Ursolic Acid Alleviates Mitotic Catastrophe in Podocyte by Inhibiting Autophagic P62 Accumulation in Diabetic Nephropathy.International journal of biological sciences · 2024Article
- Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseases.The Journal of clinical investigation · 2023Article
- New Approaches Targeting the Renin-Angiotensin System: Inhibition of Brain Aminopeptidase A, ACE2 Ubiquitination, and Angiotensinogen.The Canadian journal of cardiology · 2023Review
- Research progress on multiple cell death pathways of podocytes in diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2023Review
- Collapsing glomerulopathy: unraveling varied pathogeneses.Current opinion in nephrology and hypertension · 2023Review
- Surveying the landscape of emerging and understudied cell death mechanisms.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Urinary-derived extracellular vesicles reveal a distinct microRNA signature associated with the development and progression of Fabry nephropathy.Frontiers in medicine · 2023Article
- Elevation of effective p53 expression sensitizes wild-type p53 breast cancer cells to CDK7 inhibitor THZ1.Cell communication and signaling : CCS · 2022Article
- Emerging role of tumor suppressor p53 in acute and chronic kidney diseases.Cellular and molecular life sciences : CMLS · 2022Review
- Correlation of Ferroptosis and Other Types of Cell Death in Neurodegenerative Diseases.Neuroscience bulletin · 2022Review
- The Current Role of Dexmedetomidine as Neuroprotective Agent: An Updated Review.Brain sciences · 2021Review
- Impairment of Proteasome Function in Podocytes Leads to CKD.Journal of the American Society of Nephrology : JASN · 2021Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Murine double minute-2 (MDM2), an E3 ligase that regulates the cell cycle and inflammation, is highly expressed in podocytes. In podocyte injury, MDM2 drives podocyte loss by mitotic catastrophe, but the function of MDM2 in resting podocytes has not been explored. Here, we investigated the effects of podocyte MDM2 deletion in vitro and in vivo. In vitro, MDM2 knockdown by siRNA caused increased expression of p53 and podocyte death, which was completely rescued by coknockdown of p53. Apoptosis, pyroptosis, pyronecrosis, necroptosis, ferroptosis, and parthanatos were excluded as modes of occurrence for this p53-overactivation-related cell death (here referred to as podoptosis). Podoptosis was associated with cytoplasmic vacuolization, endoplasmic reticulum stress, and dysregulated autophagy (previously described as paraptosis). MDM2 knockdown caused podocyte loss and proteinuria in a zebrafish model, which was consistent with the phenotype of podocyte-specific MDM2-knockout mice that also showed the aforementioned ultrastructual podocyte abnormalities before and during progressive glomerulosclerosis. The phenotype of both animal models was entirely rescued by codeletion of p53. We conclude that MDM2 maintains homeostasis and long-term survival in podocytes by preventing podoptosis, a p53-regulated form of cell death with unspecific features previously classified as paraptosis.
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