ArticleEMBO molecular medicine2015
Inhibition of insulin/IGF-1 receptor signaling protects from mitochondria-mediated kidney failure.
Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 75 citations in OpenAlex.
- The insulin/IGF axis is critically important for controlling gene transcription in the podocyte.eLife · 2026Article
- Article
- Persistent mTORC1 activation underlies sex dimorphic progression of MASLD in mice with hepatocyte prohibitin-1 deficiency.Research square · 2025Article
- Inflammatory Milieu by Crosstalk between Glomerulus and Proximal Tubular Cells in Type 2 Diabetes Mellitus Kidney Disease.Diabetes & metabolism journal · 2025Article
- UBC9-Mediated SUMO Pathway Drives Prohibitin-1 Nuclear Accumulation and PITX1 Repression in Primary Osteoarthritis.International journal of molecular sciences · 2025Article
- Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage.JCI insight · 2025Article
- Profiling of insulin-resistant kidney models and human biopsies reveals common and cell-type-specific mechanisms underpinning Diabetic Kidney Disease.Nature communications · 2024Article
- Contrasting consequences of podocyte insulin-like growth factor 1 receptor inhibition.iScience · 2024Article
- PHB2 alleviates retinal pigment epithelium cell fibrosis by suppressing the AGE-RAGE pathway.Open life sciences · 2024Article
- CEST-2.2 overexpression alters lipid metabolism and extends longevity of mitochondrial mutants.EMBO reports · 2022Article
- Podocyte Bioenergetics in the Development of Diabetic Nephropathy: The Role of Mitochondria.Endocrinology · 2022Review
- IGF1R signalling is a guardian of self-tolerance restricting autoantibody production.Frontiers in immunology · 2022Article
- Mechanistic Pathogenesis of Endothelial Dysfunction in Diabetic Nephropathy and Retinopathy.Frontiers in endocrinology · 2022Review
- SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditionsFrontiers in pharmacology · 2022Article
- Nonreceptor Tyrosine Kinase c-Abl-Mediated PHB2 Phosphorylation Aggravates Mitophagy Disorder in Parkinson's Disease Model.Oxidative medicine and cellular longevity · 2022Article
- Insulin-activated store-operated CaNature communications · 2021Article
- The Mitochondrial Prohibitin (PHB) Complex inMetabolites · 2021Review
- IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates β1-integrin/FAK signalling in human podocytes.Diabetologia · 2021Article
- Paclitaxel Ameliorates Palmitate-Induced Injury in Mouse Podocytes.Medical science monitor basic research · 2020Article
- PKC downregulation upon rapamycin treatment attenuates mitochondrial disease.Nature metabolism · 2020Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction and alterations in energy metabolism have been implicated in a variety of human diseases. Mitochondrial fusion is essential for maintenance of mitochondrial function and requires the prohibitin ring complex subunit prohibitin-2 (PHB2) at the mitochondrial inner membrane. Here, we provide a link between PHB2 deficiency and hyperactive insulin/IGF-1 signaling. Deletion of PHB2 in podocytes of mice, terminally differentiated cells at the kidney filtration barrier, caused progressive proteinuria, kidney failure, and death of the animals and resulted in hyperphosphorylation of S6 ribosomal protein (S6RP), a known mediator of the mTOR signaling pathway. Inhibition of the insulin/IGF-1 signaling system through genetic deletion of the insulin receptor alone or in combination with the IGF-1 receptor or treatment with rapamycin prevented hyperphosphorylation of S6RP without affecting the mitochondrial structural defect, alleviated renal disease, and delayed the onset of kidney failure in PHB2-deficient animals. Evidently, perturbation of insulin/IGF-1 receptor signaling contributes to tissue damage in mitochondrial disease, which may allow therapeutic intervention against a wide spectrum of diseases.
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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.