ArticleInternational journal of molecular sciences2020
Apelin-13 Inhibits Methylglyoxal-Induced Unfolded Protein Responses and Endothelial Dysfunction via Regulating AMPK Pathway.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- miR‑222‑3p inhibits diabetic skin wound healing by targeting APLN.International journal of molecular medicine · 2026Article
- Lactobacillus fermentum 2-14 mitigates the cytotoxicity induced by methylglyoxal by activating the AMPK-autophagy signaling axis.NPJ science of food · 2026Article
- Piperine improves ischemic brain injury by promoting the regulation of the AMPK/PGC-1α pathway by Apelin 13.Frontiers in pharmacology · 2026Article
- Exploring Glyoxalase Strategies for Managing Sugar-Induced Chronic Diseases.Life (Basel, Switzerland) · 2025Article
- Acacetin reduces endoplasmic reticulum stress through the P-eNOS/PERK signaling pathway to attenuate MGO-induced vascular endothelial cell dysfunction.FEBS open bio · 2025Article
- Apelin/APJ alleviates diabetic nephropathy by improving glomerular endothelial cells dysfunction via SIRT3‑KLF15.Molecular medicine reports · 2025Article
- Protective effects of Apelin-13 on nicotine-induced H9c2 cardiomyocyte apoptosis and oxidative stress.Tobacco induced diseases · 2025Article
- Molecular and pathophysiological relationship between obesity and chronic inflammation in the manifestation of metabolic dysfunctions and their inflammation‑mediating treatment options (Review).Molecular medicine reports · 2024Review
- Apelin‑13 reduces high glucose‑induced mitochondrial dysfunction in cochlear hair cells by inhibiting endoplasmic reticulum stress.Experimental and therapeutic medicine · 2024Article
- Article
- Review
- ApoA-I Nanoparticles as Curcumin Carriers for Cerebral Endothelial Cells: Improved Cytoprotective Effects against Methylglyoxal.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Research Progress on Mechanism of Neuroprotective Roles of Apelin-13 in Prevention and Treatment of Alzheimer's Disease.Neurochemical research · 2022Review
- The Role of Apelin-APJ System in Diabetes and Obesity.Frontiers in endocrinology · 2022Review
- Unfolded protein response during cardiovascular disorders: a tilt towards pro-survival and cellular homeostasis.Molecular and cellular biochemistry · 2021Review
- Amidation-Modified Apelin-13 Regulates PPARBioinorganic chemistry and applications · 2021Article
- Apelin-13 Protects Dopaminergic Neurons against Rotenone-Induced Neurotoxicity through the AMPK/mTOR/ULK-1 Mediated Autophagy Activation.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
It has been suggested that methylglyoxal (MGO), a glycolytic metabolite, has more detrimental effects on endothelial dysfunction than glucose itself. Recent reports showed that high glucose and MGO induced endoplasmic reticulum (ER) stress and myocyte apoptosis in ischemic heart disease was inhibited by apelin. The goal of the study is to investigate the molecular mechanism by which MGO induces endothelial dysfunction via the regulation of ER stress in endothelial cells, and to examine whether apelin-13, a cytoprotective polypeptide ligand, protects MGO-induced aortic endothelial dysfunction. MGO-induced ER stress and apoptosis were determined by immunoblotting and MTT assay in HUVECs. Aortic endothelial dysfunction was addressed by en face immunostaining and acetylcholine-induced vasodilation analysis with aortic rings from mice treated with MGO in the presence or absence of apelin ex vivo. TUDCA, an inhibitor of ER stress, inhibited MGO-induced apoptosis and reduction of cell viability, suggesting that MGO signaling to endothelial apoptosis is mediated via ER stress, which leads to activation of unfolded protein responses (UPR). In addition, MGO-induced UPR and aortic endothelial dysfunction were significantly diminished by apelin-13. Finally, this study showed that apelin-13 protects MGO-induced UPR and endothelial apoptosis through the AMPK pathway. Apelin-13 reduces MGO-induced UPR and endothelial dysfunction via regulating the AMPK activating pathway, suggesting the therapeutic potential of apelin-13 in diabetic cardiovascular complications.
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Registered trials
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.