ArticleCell death and differentiation2025
PRDM16 deficiency promotes podocyte injury by impairing insulin receptor signaling.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- SnRNA-seq and genome-wide CRISPR screening define the complete transcriptional trajectory and functional drivers of podocyte stress.Cellular and molecular life sciences : CMLS · 2026Article
- Insulin resistance and hyperinsulinaemia in kidney disease: mechanisms and metabolic effects.Nature reviews. Nephrology · 2026Review
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
- The Inflammatory Cell Death in Diabetic Kidney Disease: Integrating Multifactorial Mechanisms into Novel Therapeutics.International journal of molecular sciences · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Impaired glucose uptake regulated by suppressed insulin receptor signaling is a key driving force of podocytopathies. The identification of potential therapeutic targets that mediate podocyte insulin receptor signaling holds significant clinical importance. Here, we observed a substantial reduction in PR domain-containing 16 (PRDM16) expression within damaged podocytes in both humans and mice. Podocyte-specific Prdm16 deletion aggravated podocyte injury, albuminuria, and glomerulosclerosis in diabetic nephropathy (DN) mice. Conversely, exogenous PRDM16 delivered by lentivirus mitigated these pathological changes in DN mice and adriamycin (ADR) nephropathy mice. Furthermore, we demonstrated that loss of PRDM16 blocked glucose uptake of podocytes by inhibiting insulin receptor signaling. Mechanistically, PRDM16 deficiency downregulated the transcription of NEDD4L, subsequently enhancing the stability of IKKβ protein. The accumulation of IKKβ caused by the loss of PRDM16 led to the phosphorylation of serine residues on insulin receptor substrate-1 (IRS-1), thereby promoting IRS-1 degradation. Exogenous NEDD4L mitigated podocyte injury induced by PRDM16 knockdown in vitro and attenuated ADR nephropathy in vivo. Our study clarified the role and mechanism of PRDM16 in insulin receptor signaling and podocyte injury, providing a potential therapeutic target for podocytopathies.
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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.