ArticlePeerJ2025
Bioinformatics-based identification of RAS disequilibrium involved in post-hemorrhagic shock mesenteric lymph return-mediated acute kidney injury in mice.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Post-hemorrhagic shock mesenteric lymph (PHSML) return plays a critical role in the development of acute kidney injury (AKI). However, the molecular mechanism underlying PHSML-mediated AKI remains unclear. In this study, bioinformatics analysis identified key common targets of hemorrhagic shock and AKI, revealing significant enrichment in the renin-angiotensin system (RAS). To further investigate the role of RAS in PHSML-mediated AKI, we established mesenteric lymph duct ligation (MLDL) technology in mice and confirmed that MLDL alleviated hemorrhagic shock-induced AKI. Subsequently, male C57BL/6 mice subjected to hemorrhagic shock were treated with the angiotensin converting enzyme (ACE) inhibitor enalapril, angiotensin (1-7) (Ang (1-7)), and angiotensin II (Ang II) type 1 receptor (AT1R) inhibitor losartan. Additionally, mice with hemorrhage and MLDL were treated with Ang II, the Mas receptor (MasR) inhibitor A-779, or subjected to
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