ArticleAmerican journal of physiology. Renal physiology2009
Human heat shock protein 27-overexpressing mice are protected against acute kidney injury after hepatic ischemia and reperfusion.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Dihydromyricetin protects against cisplatin-induced renal injury and mitochondria-mediated apoptosis via the EGFR/HSP27/STAT3 signaling pathway.Renal failure · 2025Article
- Inflammatory Gene Expression in Livers Undergoing Ex Situ Normothermic Perfusion Is Attenuated by Leukocyte Removal From the Perfusate.Transplantation · 2025Article
- NGAL in the Development of Acute Kidney Injury in a Murine Model of Remote Ischaemic Preconditioning and Liver Ischaemia Reperfusion.International journal of molecular sciences · 2024Article
- Review
- Literature review of the mechanisms of acute kidney injury secondary to acute liver injury.World journal of nephrology · 2022Review
- Aminoguanidine Prevents the Oxidative Stress, Inhibiting Elements of Inflammation, Endothelial Activation, Mesenchymal Markers, and Confers a Renoprotective Effect in Renal Ischemia and Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Article
- Renal proximal tubular NEMO plays a critical role in ischemic acute kidney injury.JCI insight · 2020Article
- Selective nanoparticle-mediated targeting of renal tubular Toll-like receptor 9 attenuates ischemic acute kidney injury.Kidney international · 2020Article
- P2X4 receptor exacerbates ischemic AKI and induces renal proximal tubular NLRP3 inflammasome signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Norepinephrine released by intestinal Paneth cells exacerbates ischemic AKI.American journal of physiology. Renal physiology · 2020Article
- Phosphorylated Heat Shock Protein 27 Inhibits Lipopolysaccharide-Induced Inflammation in Thp1 Cells by Promoting TLR4 Endocytosis, Ubiquitination, and Degradation.Inflammation · 2019Article
- 6-Shogaol protects against ischemic acute kidney injury by modulating NF-κB and heme oxygenase-1 pathways.American journal of physiology. Renal physiology · 2019Article
- Kidney Proximal Tubular TLR9 Exacerbates Ischemic Acute Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- A1AR-mediated renal protection against ischemia/reperfusion injury is dependent on HSP27 induction.International urology and nephrology · 2018Article
- Impact of Mitochondrial Permeability on Endothelial Cell Immunogenicity in Transplantation.Transplantation · 2018Article
- Divergent roles for kidney proximal tubule and granulocyte PAD4 in ischemic AKI.American journal of physiology. Renal physiology · 2018Article
- Nitrolipids in kidney physiology and disease.Nitric oxide : biology and chemistry · 2018Review
- LPS ameliorates renal ischemia/reperfusion injury via Hsp27 up-regulation.International urology and nephrology · 2018Article
- Cerium oxide nanoparticles attenuate acute kidney injury induced by intra-abdominal infection in Sprague-Dawley rats.Journal of nanobiotechnology · 2015Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Liver ischemia-reperfusion injury (IRI) causes acute kidney injury (AKI) in mice characterized by renal endothelial cell apoptosis, renal tubular necrosis, inflammation, and filamentous (F)-actin disruption. Since heat shock protein 27 (HSP27) protects against apoptosis, necrosis, and stabilizes F-actin, we questioned whether overexpression of human HSP27 (huHSP27 OE) in mice would attenuate AKI after liver IRI. Twenty-four hours after hepatic IRI, HSP27 wild-type (WT) mice developed acute liver and kidney injury with elevated plasma alanine aminotransferase and creatinine, a reduced glomerular filtration rate, and histological evidence of renal endothelial cell apoptosis and tubular injury (necrosis, vacuolization, and F-actin disruption). The huHSP27 OE mice, however, were significantly protected against both liver and kidney injury after hepatic IRI. The huHSP27 OE mice also showed less induction of several proinflammatory mRNAs (TNF-alpha, MIP-2, and keratinocyte-derived cytokine), neutrophil infiltration, and reduction in apoptosis (terminal deoxynucleotidyl transferase biotin-dUTP nick end-labeling assay and DNA laddering) in the kidney compared with the HSP27 WT mice. Moreover, the huHSP27 OE mice showed significantly less disruption of F-actin in renal proximal tubules and better preserved vascular endothelial cell integrity compared with the huHSP27 OE mice. Finally, the kidney plays a major role in the hepatoprotective effects of huHSP27 overexpression as the hepatoprotection was reduced or abolished in mice subjected to unilateral or bilateral nephrectomy, respectively. Our results show that overexpression of huHSP27 protects against hepatic injury and AKI associated with liver IRI in vivo. Harnessing the mechanisms of cytoprotection with renal HSP27 may lead to new therapies for the perioperative AKI and liver injury associated with liver IRI.
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