ArticleInternational journal of molecular sciences2024
Cadmium Induces Vascular Endothelial Cell Detachment by Downregulating Claudin-5 and ZO-1 Levels.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Cadmium chloride administered through drinking water disrupts the gut-liver axis through intestinal barrier failure, endoplasmic reticulum stress, and PIEZO1 signaling in broiler chickens.Poultry science · 2026Article
- Genomic Impacts of Biological Exposures.Journal of developmental biology · 2026Review
- Liver sinusoidal endothelial cells secret C-X-C motif chemokine ligand 10 to promote the recruitment of invariant NKT cells in acetaminophen-induced liver injury.Science China. Life sciences · 2025Article
- Association Between Blood Cadmium Levels and Heart Failure Risk: Insights From NHANES 2009-2014.Cardiovascular therapeutics · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Cadmium is a contributing factor to cardiovascular diseases and highly toxic to vascular endothelial cells. It has a distinct mode of injury, causing the de-endothelialization of regions in the monolayer structure of endothelial cells in a concentration-dependent manner. However, the specific molecules involved in the cadmium toxicity of endothelial cells remain unclear. The purpose of this study was to identify the specific molecular mechanisms through which cadmium affects endothelial detachment. Cadmium inhibited the expression of claudin-5 and zonula occludens (ZO)-1, which are components of tight junctions (strongest contributors to intercellular adhesion), in a concentration- and time-dependent manner. Compared to arsenite, zinc, and manganese, only cadmium suppressed the expression of both claudin-5 and ZO-1 molecules. Moreover, the knockdown of claudin-5 and ZO-1 exacerbated cadmium-induced endothelial cell injury and expansion of the detachment area, whereas their overexpression reversed these effects. CRE-binding protein inhibition reduced cadmium toxicity, suggesting that CRE-binding protein activation is involved in the cadmium-induced inhibition of claudin-5 and ZO-1 expression and endothelial detachment. These findings provide new insights into the toxicological mechanisms of cadmium-induced endothelial injury and risk of cardiovascular disease.
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Registered trials
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