ArticleScientific reports2018
Enhanced insulin receptor, but not PI3K, signalling protects podocytes from ER stress.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Lycopene Attenuates Hexavalent Chromium-Induced Hepatotoxicity in Mice by Modulating the Nrf2 Signaling Pathway and the Unfolded Protein Response.Biological trace element research · 2026Article
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Advances regarding the mechanism of endoplasmic reticulum stress in diabetic kidney disease and pharmacological interventions (Review).Molecular medicine reports · 2026Review
- Risk factors for progression to albuminuria in individuals with newly diagnosed type 2 diabetes: a 5-year cohort study.BMC endocrine disorders · 2025Observational
- The Role of miRNAs as Early Biomarkers in Obesity-Related Glomerulopathy: Implications for Early Detection and Treatment.Biomedicines · 2025Review
- Targeting endoplasmic reticulum stress: an innovative therapeutic strategy for podocyte-related kidney diseases.Journal of translational medicine · 2025Review
- Article
- Profiling of insulin-resistant kidney models and human biopsies reveals common and cell-type-specific mechanisms underpinning Diabetic Kidney Disease.Nature communications · 2024Article
- Endoplasmic reticulum stress in diabetic kidney disease: adaptation and apoptosis after three UPR pathways.Apoptosis : an international journal on programmed cell death · 2023Review
- Identification of endoplasmic reticulum stress-related biomarkers of diabetes nephropathy based on bioinformatics and machine learning.Frontiers in endocrinology · 2023Article
- Effect of chitooligosaccharides with a specific degree of polymerization on multiple targets in T2DM mice.Bioresources and bioprocessing · 2022Article
- The role of protein tyrosine phosphatase 1B (PTP1B) in the pathogenesis of type 2 diabetes mellitus and its complications.Journal of physiology and biochemistry · 2022Review
- International retrospective study of allogeneic hematopoietic cell transplantation for activated PI3K-delta syndrome.The Journal of allergy and clinical immunology · 2022Article
- Screening and Identification of Hub Genes in the Development of Early Diabetic Kidney Disease Based on Weighted Gene Co-Expression Network Analysis.Frontiers in endocrinology · 2022Article
- IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates β1-integrin/FAK signalling in human podocytes.Diabetologia · 2021Article
- Scientific Advances in Diabetes: The Impact of the Innovative Medicines Initiative.Frontiers in medicine · 2021Review
- Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020Review
- SHIPping out diabetes-Metformin, an old friend among new SHIP2 inhibitors.Acta physiologica (Oxford, England) · 2020Review
- The Evolving Importance of Insulin Signaling in Podocyte Health and Disease.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Disruption of the insulin-PI3K-Akt signalling pathway in kidney podocytes causes endoplasmic reticulum (ER) stress, leading to podocyte apoptosis and proteinuria in diabetic nephropathy. We hypothesised that by improving insulin sensitivity we could protect podocytes from ER stress. Here we use established activating transcription factor 6 (ATF6)- and ER stress element (ERSE)-luciferase assays alongside a novel high throughput imaging-based C/EBP homologous protein (CHOP) assay to examine three models of improved insulin sensitivity. We find that by improving insulin sensitivity at the level of the insulin receptor (IR), either by IR over-expression or by knocking down the negative regulator of IR activity, protein tyrosine-phosphatase 1B (PTP1B), podocytes are protected from ER stress caused by fatty acids or diabetic media containing high glucose, high insulin and inflammatory cytokines TNFα and IL-6. However, contrary to this, knockdown of the negative regulator of PI3K-Akt signalling, phosphatase and tensin homolog deleted from chromosome 10 (PTEN), sensitizes podocytes to ER stress and apoptosis, despite increasing Akt phosphorylation. This indicates that protection from ER stress is conferred through not just the PI3K-Akt pathway, and indeed we find that inhibiting the MEK/ERK signalling pathway rescues PTEN knockdown podocytes from ER stress.
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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.