ArticleJournal of physiology and biochemistry2015
Advanced oxidation protein products induce apoptosis in podocytes through induction of endoplasmic reticulum stress.
Article in Journal of physiology and biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Stromal Cell-Derived Factor-1, P-Selectin, and Advanced Oxidation Protein Products with Mitochondrial Dysfunction Concurrently Impact Cerebral Vessels in Patients with Normoalbuminuric Diabetic Kidney Disease and Type 2 Diabetes Mellitus.International journal of molecular sciences · 2025Article
- Targeting endoplasmic reticulum stress: an innovative therapeutic strategy for podocyte-related kidney diseases.Journal of translational medicine · 2025Review
- Damage-Associated Molecular Patterns and Pattern Recognition Receptors in the Podocyte.Journal of the American Society of Nephrology : JASN · 2025Review
- Post-translational modifications in kidney diseases and associated cardiovascular risk.Nature reviews. Nephrology · 2024Review
- Article
- Advanced oxidation protein products induce Paneth cells defects by endoplasmic reticulum stress in Crohn's disease.iScience · 2023Article
- Peroxiredoxin-4 and Dopamine D5 Receptor Interact to Reduce Oxidative Stress and Inflammation in the Kidney.Antioxidants & redox signaling · 2023Article
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- LCZ696 Protects against Diabetic Cardiomyopathy-Induced Myocardial Inflammation, ER Stress, and Apoptosis through Inhibiting AGEs/NF-κB and PERK/CHOP Signaling Pathways.International journal of molecular sciences · 2022Article
- The role of extracellular vesicles in podocyte autophagy in kidney disease.Journal of cell communication and signaling · 2021Review
- Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.Nature communications · 2021Article
- 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
- Contribution of RAGE axis activation to the association between metabolic syndrome and cancer.Molecular and cellular biochemistry · 2021Review
- Beta carotene protects H9c2 cardiomyocytes from advanced glycation end product-induced endoplasmic reticulum stress, apoptosis, and autophagy via the PI3K/Akt/mTOR signaling pathway.Annals of translational medicine · 2020Article
- Association of Higher Advanced Oxidation Protein Products (AOPPs) Levels in Patients with Diabetic and Hypertensive Nephropathy.Medicina (Kaunas, Lithuania) · 2019Article
- Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne's Thread.International journal of molecular sciences · 2019Review
- Deletion of the formin Diaph1 protects from structural and functional abnormalities in the murine diabetic kidney.American journal of physiology. Renal physiology · 2018Article
- APOL1 risk variants cause podocytes injury through enhancing endoplasmic reticulum stress.Bioscience reports · 2018Article
- Advanced oxidation protein products from the follicular microenvironment and their role in infertile women with endometriosis.Experimental and therapeutic medicine · 2018Article
- Mito-TEMPO Alleviates Renal Fibrosis by Reducing Inflammation, Mitochondrial Dysfunction, and Endoplasmic Reticulum Stress.Oxidative medicine and cellular longevity · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although podocyte apoptosis has been shown to be induced by the accumulation of advanced oxidation protein products (AOPPs), the mechanisms through which AOPPs trigger apoptosis in these cells remain unclear. In this study, we investigated the role of endoplasmic reticulum (ER) stress in AOPP-induced podocyte apoptosis. AOPP treatment induced overexpression of glucose-regulated protein 78 and CCAAT/enhancer-binding protein-homologous protein (CHOP) in podocytes, indicating that AOPPs induced ER stress. Notably, AOPP-induced increase in the rate of podocyte apoptosis was partly reversed by salubrinal, an ER stress inhibitor, whereas the AOPP effect was reproduced by an inducer of ER stress, thapsigargin, suggesting that AOPPs triggered podocyte apoptosis by inducing ER stress. Furthermore, AOPP-induced reactive oxygen species (ROS) generation, ER stress, and podocyte apoptosis were significantly inhibited by an nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, a ROS scavenger, or receptor of advanced glycation end products (RAGE) small interfering RNA (siRNA). Moreover, silencing of the three ER stress sensors, protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), and inositol requiring 1 (IRE1), respectively, significantly lowered the apoptotic rate of the cells compared with that of the scramble siRNA-transfected cells. Lastly, our data suggested that CHOP- and caspase-12-dependent pathways were involved in ER stress-mediated podocyte apoptosis and that Bcl-2 suppression was involved in CHOP-mediated apoptosis. Collectively, our results indicate for the first time that AOPPs trigger podocyte apoptosis through induction of ER stress, which might be regulated by NADPH oxidase-dependent ROS through RAGE, and that this apoptosis is mediated by three unfolded protein response pathways, the PERK, ATF6, and IRE1 pathways, and the mediators, CHOP and caspase-12.
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