ArticleMolecular biology of the cell2017
Deletion of inositol-requiring enzyme-1α in podocytes disrupts glomerular capillary integrity and autophagy.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- EVA1A responds to endoplasmic reticulum stress to regulate renal fibrosis by promoting TGF-β signaling pathway.Journal of advanced research · 2026Article
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
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- ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice.Scientific reports · 2024Article
- Deletion of IRE1α in podocytes exacerbates diabetic nephropathy in mice.Scientific reports · 2024Article
- Article
- Beyond UPR: cell-specific roles of ER stress sensor IRE1α in kidney ischemic injury and transplant rejection.Kidney international · 2023Review
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- Endoplasmic Reticulum Stress in Systemic Lupus Erythematosus and Lupus Nephritis: Potential Therapeutic Target.Journal of immunology research · 2023Review
- Regulation of the Homeostatic Unfolded Protein Response in Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond.Frontiers in molecular medicine · 2022Review
- Diabetic nephropathy in mice is aggravated by the absence of podocyte IRE1 and is correlated with reduced kidney ADH1 expression.Annals of translational medicine · 2021Article
- Endoplasmic reticulum-associated degradation is required for nephrin maturation and kidney glomerular filtration function.The Journal of clinical investigation · 2021Article
- Endoplasmic Reticulum-Associated Biomarkers for Molecular Phenotyping of Rare Kidney Disease.International journal of molecular sciences · 2021Review
- Mfn2 Regulates High Glucose-Induced MAMs Dysfunction and Apoptosis in PodocytesFrontiers in cell and developmental biology · 2021Article
- Role of IRE1α in podocyte proteostasis and mitochondrial health.Cell death discovery · 2020Article
- Organelle Stress and Crosstalk in Kidney Disease.Kidney360 · 2020Review
- Urinary ERdj3 and mesencephalic astrocyte-derived neutrophic factor identify endoplasmic reticulum stress in glomerular disease.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- The cellular prion protein is a stress protein secreted by renal tubular cells and a urinary marker of kidney injury.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inositol-requiring enzyme-1α (IRE1α) is an endoplasmic reticulum (ER)-transmembrane endoribonuclease kinase that plays an essential function in extraembryonic tissues during normal development and is activated during ER stress. To address the functional role of IRE1α in glomerular podocytes, we produced podocyte-specific IRE1α-deletion mice. In male mice, deletion of IRE1α in podocytes resulted in albuminuria beginning at 5 mo of age and worsening with time. Electron microscopy revealed focal podocyte foot-process effacement in 9-mo-old male IRE1α-deletion mice, as well as microvillous transformation of podocyte plasma membranes. Compared with control, glomerular cross-sectional and capillary lumenal areas were greater in deletion mice, and there was relative podocyte depletion. Levels of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II expression and c-Jun N-terminal kinase-1 phosphorylation were decreased in IRE1α-deletion glomeruli, in keeping with reduced autophagy. Deletion of IRE1α exacerbated glomerular injury in anti-glomerular basement membrane nephritis. In cell culture, IRE1α dominant-negative mutants reduced the physiological (basal) accumulation of LC3B-II and the size of autophagic vacuoles but did not affect ER-associated degradation. Thus IRE1α is essential for maintaining podocyte and glomerular integrity as mice age and in glomerulonephritis. The mechanism is related, at least in part, to the maintenance of autophagy in podocytes.
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