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SGLT2 inhibition ameliorates nano plastics-induced premature endothelial senescence and dysfunction
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Researchers found that nanoplastics cause premature aging and dysfunction in blood vessel lining cells, and that an SGLT2 inhibitor drug could help counteract these effects. The nanoplastics triggered oxidative stress and inflammation in endothelial cells, which are linked to cardiovascular problems. The study suggests a potential therapeutic approach to address some of the vascular damage associated with nanoplastic exposure.
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. Furthermore, SGLT2 inhibition also up regulated the endothelial nitric oxide synthase expression along with improving vascular function. In conclusion, premature endothelial senescence by NPs is, at least in part, associated with SGLT2 and it could be a potential therapeutic target for preventing and/or treating environmental pollutants-induced cardiovascular disorders mediated by endothelial senescence and dysfunction.
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Abstract 10442: Protective Effect of Inhibition of Sglt2 on Nanoplastics-Induced Premature Endothelial Senescence and Dysfunction
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Researchers investigated whether SGLT2 inhibition (gliflozins) protects against nanoplastic-induced premature endothelial senescence and dysfunction, using porcine coronary artery rings and cultured endothelial cells to examine a redox-sensitive signaling pathway through which nanoplastics impair cardiovascular endothelial health.
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Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Exposure to polystyrene nanoplastics provokes vascular endothelial senescence through eliciting nucleolar stress
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Tiny plastic particles called nanoplastics—found widely in our environment—may damage the cells lining our blood vessels, causing them to age faster than normal, according to a study in mice and human cells. The plastics triggered stress inside cells that led to premature aging of blood vessel walls, though antioxidants and certain drugs were able to block this damage in the lab. While this research is still in early stages (animal and cell models, not yet in humans), it adds to growing concerns that microplastic pollution could contribute to heart and blood vessel problems.
Effects of micro- and nano-plastics exposure on cellular senescence: an overview.
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Researchers review how micro- and nanoplastics trigger cellular senescence — a state of permanent cell cycle arrest — through oxidative stress and DNA damage, activating pathways like cGAS-STING and NF-κB that elevate risk for age-related diseases, and survey potential therapeutic strategies to counter these effects.
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This review examines how microplastics may contribute to vascular aging and cardiovascular problems. Evidence indicates that once microplastics enter the body through ingestion, inhalation, or skin contact, they can reach blood vessels and trigger oxidative stress, inflammation, and damage to the cells lining blood vessel walls. The findings suggest that chronic microplastic exposure could be an underappreciated factor in the development of age-related cardiovascular issues.
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