ArticleScientific reports2016
Involvement of Endoplasmic Reticulum Stress, Autophagy, and Apoptosis in Advanced Glycation End Products-Induced Glomerular Mesangial Cell Injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Autophagy in kidney physiology: from cellular quality control to organ metabolism.Autophagy reports · 2026Review
- The role of glucagon-like peptide-1/GLP-1R and autophagy in diabetic cardiovascular disease.Pharmacological reports : PR · 2024Review
- PHB2 alleviates retinal pigment epithelium cell fibrosis by suppressing the AGE-RAGE pathway.Open life sciences · 2024Article
- Chinese botanical drugs targeting mitophagy to alleviate diabetic kidney disease, a comprehensive review.Frontiers in pharmacology · 2024Review
- SARS-CoV-2 nonstructural protein 6 triggers endoplasmic reticulum stress-induced autophagy to degrade STING1.Autophagy · 2023Article
- Beyond Glucose: The Dual Assault of Oxidative and ER Stress in Diabetic Disorders.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2023Review
- Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.American journal of physiology. Renal physiology · 2023Review
- Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy.Journal of diabetes research · 2023Review
- The role of Chinese herbal medicine in the treatment of diabetic nephropathy by regulating endoplasmic reticulum stress.Frontiers in pharmacology · 2023Review
- Involvement of endoplasmic reticulum stress and cell death by synthesized Pa-PDT in oral squamous cell carcinoma cells.Journal of dental sciences · 2022Article
- Glycolaldehyde, an Advanced Glycation End Products Precursor, Induces Apoptosis via ROS-Mediated Mitochondrial Dysfunction in Renal Mesangial Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Regulation of the Homeostatic Unfolded Protein Response in Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Effects ofExperimental and therapeutic medicine · 2021Article
- Exosomes Immunity Strategy: A Novel Approach for Ameliorating Intervertebral Disc Degeneration.Frontiers in cell and developmental biology · 2021Review
- Interactions between Endoplasmic Reticulum Stress and Autophagy: Implications for Apoptosis and Neuroplasticity-Related Proteins in Palmitic Acid-Treated Prefrontal Cells.Neural plasticity · 2021Article
- Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies.Biomedicines · 2020Review
- LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition.Annals of translational medicine · 2020Article
- Lysosomal dysfunction-induced autophagic stress in diabetic kidney disease.Journal of cellular and molecular medicine · 2020Review
- Phenylbutyrate facilitates homeostasis of non-resolving inflammatory macrophages.Innate immunity · 2020Article
- Autophagy Activation is Associated with Neuroprotection in Diabetes-associated Cognitive Decline.Aging and disease · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end-products (AGEs)-induced mesangial cell death is one of major causes of glomerulus dysfunction in diabetic nephropathy. Both endoplasmic reticulum (ER) stress and autophagy are adaptive responses in cells under environmental stress and participate in the renal diseases. The role of ER stress and autophagy in AGEs-induced mesangial cell death is still unclear. Here, we investigated the effect and mechanism of AGEs on glomerular mesangial cells. AGEs dose-dependently decreased mesangial cell viability and induced cell apoptosis. AGEs also induced ER stress signals in a time- and dose-dependent manner. Inhibition of ER stress with 4-phenylbutyric acid effectively inhibited the activation of eIF2α and CHOP signals and reversed AGEs-induced cell apoptosis. AGEs also activated LC-3 cleavage, increased Atg5 expression, and decreased p62 expression, which indicated the autophagy induction in mesangial cells. Inhibition of autophagy by Atg5 siRNAs transfection aggravated AGEs-induced mesangial cell apoptosis. Moreover, ER stress inhibition by 4-phenylbutyric acid significantly reversed AGEs-induced autophagy, but autophagy inhibition did not influence the AGEs-induced ER stress-related signals activation. These results suggest that AGEs induce mesangial cell apoptosis via an ER stress-triggered signaling pathway. Atg5-dependent autophagy plays a protective role. These findings may offer a new strategy against AGEs toxicity in the kidney.
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