ArticleCell death & disease2018
Pancreatic β cells overexpressing hIAPP impaired mitophagy and unbalanced mitochondrial dynamics.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Combined training and hormones/enzymes with insulinotropic actions in individuals with overweight and type 2 diabetes mellitus: A randomized controlled trial.European journal of sport science · 2024Trial
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Highly Sensitive Water-Soluble Donor-Acceptor Dye for Early-Stage Amyloid Aggregation Kinetics.The journal of physical chemistry. B · 2026Article
- Resveratrol modulates pancreatic proteotoxic stress and metabolic dysfunction in human IAPP transgenic mice.Frontiers in endocrinology · 2026Article
- Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies.Cell death & disease · 2025Review
- Resveratrol protects pancreatic beta cell and hippocampal cells from the aggregate-prone capacity of hIAPP.Scientific reports · 2024Article
- The overexpression of human amylin in pancreatic β cells facilitate the appearance of amylin aggregates in the kidney contributing to diabetic nephropathy.Scientific reports · 2024Article
- Regulation of TSC2 lysosome translocation and mitochondrial turnover by TSC2 acetylation status.Scientific reports · 2024Article
- The crosstalk between mitochondrial quality control and metal-dependent cell death.Cell death & disease · 2024Review
- Extracellular vesicle-mediated intercellular and interorgan crosstalk of pancreatic islet in health and diabetes.Frontiers in endocrinology · 2023Review
- Mitochondrial proteotoxicity: implications and ubiquitin-dependent quality control mechanisms.Cellular and molecular life sciences : CMLS · 2022Review
- Human islet amyloid polypeptide: A therapeutic target for the management of type 2 diabetes mellitus.Journal of pharmaceutical analysis · 2022Review
- Article
- Urolithin B: Two-way attack on IAPP proteotoxicity with implications for diabetes.Frontiers in endocrinology · 2022Article
- Targeting pancreatic beta cell death in type 2 diabetes by polyphenols.Frontiers in endocrinology · 2022Review
- The role of mTOR in age-related diseases.Journal of enzyme inhibition and medicinal chemistry · 2021Review
- The Emerging Roles of Autophagy in Human Diseases.Biomedicines · 2021Review
- Human Islet Amyloid Polypeptide Overexpression in INS-1E Cells Influences Amylin Oligomerization under ER Stress and Oxidative Stress.International journal of molecular sciences · 2021Article
- Mitochondrial Dysfunction and Mitophagy Closely Cooperate in Neurological Deficits Associated with Alzheimer's Disease and Type 2 Diabetes.Molecular neurobiology · 2021Review
- 4-Phenylbutyrate (PBA) treatment reduces hyperglycemia and islet amyloid in a mouse model of type 2 diabetes and obesity.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human islet amyloid polypeptide (hIAPP), or amylin, has the tendency to aggregate into insoluble amyloid fibrils, a typical feature of islets from type 2 diabetes individuals. Thus, we investigated comparatively the impact of hIAPP on key pathways involved in pancreatic beta survival. INS1E-hIAPP cells present a hyperactivation of MTORC1 and an inhibition of autophagy signaling, those cells showing an increase in cell size. Resveratrol, a MTORC1 inhibitor, can reverse TSC2 degradation that occurs in INS1E-hIAPP cells and diminished MTORC1 hyperactivation with concomitant autophagy stimulation. At the same time, a blockade in mitophagy was found in INS1E-hIAPP cells, as compared with control or INS1E-rIAPP cells. Consistently, human amylin overexpression generates a basal induction of nitrotyrosine levels and polyubiquitinated aggregates. Failure of the protein degradation machinery finally results in an accumulation of damaged and fissioned mitochondria, ROS production, and increased susceptibility to endoplasmic reticulum (ER)-stress-induced apoptosis. Overall, hIAPP overexpression in INS1E cells induced MTORC1 activation and mitophagy inhibition, favoring a pro-fission scenario of damaged mitochondria, these cells turn out to be more susceptible to the ER-stress-induced apoptosis and malfunction.
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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.