ArticleCell death & disease2021
An interplay between UCP2 and ROS protects cells from high-salt-induced injury through autophagy stimulation.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 45 citations in OpenAlex.
- Beneficial Role of Resveratrol on Oxidative Stress in Women with Polycystic Ovary Syndrome: A Randomized Controlled Trial.Reproductive sciences (Thousand Oaks, Calif.) · 2025Trial
- Angiotensin II and cAMP signaling pathways regulate mitochondrial biogenesis and activity in human adrenocortical cells.Journal of the Endocrine Society · 2026Article
- Autophagy and Mitophagy in Hypertensive Chronic Kidney Disease: Evidence Grading, Cell-Type Divergence, and a Working Lysosomal Hypothesis.Life (Basel, Switzerland) · 2026Review
- Suppression of UCP2 alleviates leukemogenesis by enhancing branched-chain amino acids-induced oxidative stress via activating the PI3K/AKT/mTOR signaling pathway.Genes & diseases · 2026Article
- Autophagy in ischemic stroke: from cellular survival mechanism to pathological damage.Metabolic brain disease · 2026Review
- Sarco/Endoplasmic Reticulum CaJournal of the American Heart Association · 2026Article
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- Crosstalk between microRNAs and autophagy in adipocyte differentiation: emerging therapeutic targets for obesity.Adipocyte · 2025Review
- Mechanism Analysis of UCP2 During the Oxidative Stress Injury of Intestinal Porcine Epithelial Cell Line-J2.Animals : an open access journal from MDPI · 2025Article
- Exploring the Regulatory Effect of Hydroxytyrosol on Ovarian Inflammaging Through Autophagy-Targeted Mechanisms: A Bioinformatics Approach.Nutrients · 2025Article
- Dietary salt promotes cognitive impairment through repression of SIRT3/PINK1-mediated mitophagy and fission.Molecular and cellular biochemistry · 2025Article
- Altered leptin signaling and attenuated cardiac vagal activity in rats with type 2 diabetes.Frontiers in physiology · 2025Article
- Metformin Ameliorates Ulcerative Colitis Through Inhibiting NLRP3 Inflammasome Activation.Journal of inflammation research · 2025Article
- Emerging role and the signaling pathways of uncoupling protein 2 in kidney diseases.Renal failure · 2024Review
- Oscillatory hypoxia induced gene expression predicts low survival in human breast cancer patients.Molecular carcinogenesis · 2024Article
- Repurposed genipin targeting UCP2 exhibits antitumor activity through inducing ferroptosis in glioblastoma.Acta biochimica et biophysica Sinica · 2024Article
- The role of uncoupling protein 2 in experimental periodontitis-associated renal injury in rats.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024Article
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- UCP2, a Member of the Mitochondrial Uncoupling Proteins: An Overview from Physiological to Pathological Roles.Biomedicines · 2024Review
- High salt diet induces cognitive impairment and is linked to the activation of IGF1R/mTOR/p70S6K signaling.Metabolic brain disease · 2024Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial uncoupling protein 2 (UCP2) plays a protective function in the vascular disease of both animal models and humans. UCP2 downregulation upon high-salt feeding favors vascular dysfunction in knock-out mice, and accelerates cerebrovascular and renal damage in the stroke-prone spontaneously hypertensive rat. Overexpression of UCP2 counteracts the negative effects of high-salt feeding in both animal models. We tested in vitro the ability of UCP2 to stimulate autophagy and mitophagy as a mechanism mediating its protective effects upon high-salt exposure in endothelial and renal tubular cells. UCP2 silencing reduced autophagy and mitophagy, whereas the opposite was true upon UCP2 overexpression. High-salt exposure increased level of reactive oxygen species (ROS), UCP2, autophagy and autophagic flux in both endothelial and renal tubular cells. In contrast, high-salt was unable to induce autophagy and autophagic flux in UCP2-silenced cells, concomitantly with excessive ROS accumulation. The addition of an autophagy inducer, Tat-Beclin 1, rescued the viability of UCP2-silenced cells even when exposed to high-salt. In summary, UCP2 mediated the interaction between high-salt-induced oxidative stress and autophagy to preserve viability of both endothelial and renal tubular cells. In the presence of excessive ROS accumulation (achieved upon UCP2 silencing and high-salt exposure of silenced cells) autophagy was turned off. In this condition, an exogenous autophagy inducer rescued the cellular damage induced by excess ROS level. Our data confirm the protective role of UCP2 toward high-salt-induced vascular and renal injury, and they underscore the role of autophagy/mitophagy as a mechanism counteracting the high-salt-induced oxidative stress damage.
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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.