ArticleMolecular biotechnology2025
Understanding Propofol's Protective Mechanism in Tubular Epithelial Cells: Mitigating Pyroptosis via the miR-143-3p/ATPase Na + /K + Transporting Subunit Alpha 2 Pathway in Renal Ischemia-Reperfusion.
Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Molecular mechanism of propofol in reducing kidney injury induced by autologous orthotopic liver transplantation.Frontiers in immunology · 2026Article
- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Propofol (Pro), a prevalent intravenous anesthetic, has recently been recognized for its potential in mitigating ischemia-reperfusion (I/R) injuries. Despite a plethora of evidence suggesting the beneficial effects of low-dose Pro in renal I/R injury (RI/R), its role in modulating pyroptosis in renal tubular epithelial cells consequent to RI/R has not been thoroughly elucidated. In our investigation, we explored the therapeutic potential of Pro against pyroptosis in renal tubular epithelial cells under the duress of RI/R, employing both in vivo and in vitro models, while deciphering the intricate molecular pathways involved. Our results demonstrate an elevation in the expression of miR-143-3p, contrasted by a diminution in ATPase Na + /K + Transporting Subunit Alpha 2 (ATP1A2) under RI/R conditions. Pro effectively mitigates apoptosis in renal tubular epithelial cells induced by RI/R, principally characterized by the inhibition of pro-inflammatory cytokines interleukin (IL-)-1β and IL-18, enhancement of cellular viability, reduction in the ratio of pyroptotic cells, and suppression of nucleotide-binding domain and leucine-rich repeat-related family, pyrin domain containing 3 inflammasome activation along with the expression of cleaved caspase-1, and gasdermin D. Both knockdown and overexpression studies of miR-143-3p revealed its pivotal role in modulating RI/R-induced tubular cell pyroptosis. Notably, Pro's capacity to inhibit pyroptosis in renal tubular epithelial cells was found to be reversible following ATP1A2 knockdown. Furthermore, our study unveils miR-143-3p as a targeted regulator of ATP1A2 expression. From a mechanistic standpoint, Pro's therapeutic efficacy is attributed to its regulatory influence on miR-143-3p and ATP1A2 expression levels. In conclusion, our findings pioneer the understanding that Pro can significantly ameliorate pyroptosis in renal tubular epithelial cells in the context of RI/R, predominantly through the modulation of the miR-143-3p/ATP1A2 axis. This novel insight furnishes robust empirical support for the development of targeted therapeutics and clinical strategies in addressing RI/R.
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