ArticleScientific reports2023
SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Migration-driven exposome reconfiguration: a predictive, preventive and personalized medicine perspective on cardiometabolic risk.The EPMA journal · 2026Review
- Engineering etiology-aligned in vitro models of human vessels.Microsystems & nanoengineering · 2026Review
- Micro- and Nanoplastics in Cardiovascular Toxicology: Human Tissue Detection, Clinical Phenotypes, and Adverse Outcome Signals.Cardiovascular toxicology · 2026Review
- Effects of micro- and nano-plastics exposure on cellular senescence: an overview.Archives of toxicology · 2026Review
- Micro-nanoplastics in Cardiovascular Disease: A Critical Update from Environmental Exposure to Clinical Implications.Cardiovascular toxicology · 2026Review
- Endothelial Senescence Drives Deleterious Endothelial-Adipocyte Cross-Talk in Patients With Heart Failure and Type 2 Diabetes.JACC. Basic to translational science · 2026Article
- Microplastics induce mitochondrial dysfunction and accelerate cardiovascular pathogenesis.Archives of toxicology · 2026Review
- Microplastics and Nanoplastics in Cardiovascular Disease: An Emerging Cardiovascular Risk Factor.Cardiovascular toxicology · 2026Review
- γ-Oryzanol Ameliorates Endothelial Replicative Senescence via Downregulation of SGLT2 Expression to Attenuate NADPH-Driven Oxidative Stress.Biomolecules & therapeutics · 2026Article
- Emerging cardiovascular risks of micro- and nanoplastics: toxic effects and mechanistic pathways.Particle and fibre toxicology · 2026Review
- Micro-nanoplastic induced cardiovascular disease and dysfunction: a scoping review.Journal of exposure science & environmental epidemiology · 2025Article
- Beneficial and challenges of exosome application in ischemic heart disease.Stem cell research & therapy · 2025Review
- SGLT2 inhibitors as a novel senotherapeutic approach.npj aging · 2025Review
- Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease.Molecular and cellular biochemistry · 2025Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease Induced by Microplastics: An Endpoint in the Liver-Eye Axis.International journal of molecular sciences · 2025Review
- Impact of sodium-glucose cotransporter-2 inhibitors on pulmonary vascular cell function and arterial remodeling.World journal of cardiology · 2025Review
- Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence.Cells · 2024Review
- Micro-nanoplastics and cardiovascular diseases: evidence and perspectives.European heart journal · 2024Review
- Young hearts at risk: Unveiling novel factors in myocardial infarction susceptibility and prevention.Journal of family medicine and primary care · 2024Review
- An Emerging Role of Micro- and Nanoplastics in Vascular Diseases.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nano plastics (NPs) have been a significant threat to human health and are known to cause premature endothelial senescence. Endothelial senescence is considered one of the primary risk factors contributing to numerous cardiovascular disorders. Recent studies have suggested that inhibition of sodium glucose co-transporter (SGLT2) ameliorates endothelial senescence and dysfunction. Therefore, our study intends to explore the role of SGLT2 in NPs-induced endothelial senescence and dysfunction. Porcine coronary artery and its endothelial cells were treated with NPs in the presence or absence of Enavogliflozin (ENA), a SGLT2 inhibitor and then SGLTs expression, senescence markers and vascular function were evaluated. NPs significantly up-regulated SGLT2 and ENA significantly decreased NPs-induced senescence-associated-β-gal activity, cell-cycle arrest, and senescence markers p53 and p21 suggesting that inhibition of SGLT2 prevents NPs-induced endothelial senescence. In addition, ENA decreased the formation of reactive oxygen species with the downregulation of Nox2, and p22
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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.