ArticleAmerican journal of physiology. Renal physiology2012
Overexpression of cGMP-dependent protein kinase I (PKG-I) attenuates ischemia-reperfusion-induced kidney injury.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Zhuangyang Bushen Pill Attenuates Renal Injury in Chronic Glomerulonephritis by Suppressing the MAPK Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- C-Type Natriuretic Peptide Plays an Anti-Inflammatory Role in Rat Epididymitis Induced byFrontiers in cellular and infection microbiology · 2021Article
- Depletion of cyclic-GMP levels and inhibition of cGMP-dependent protein kinase activate p21FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The phosphodiesterase 5 inhibitor tadalafil has renoprotective effects in a rat model of chronic kidney disease.Physiological reports · 2020Article
- Osteocrin attenuates inflammation, oxidative stress, apoptosis, and cardiac dysfunction in doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2020Article
- cGMP-dependent protein kinase I in vascular smooth muscle cells improves ischemic stroke outcome in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- CRRL269.Circulation research · 2019Article
- Particulate Guanylyl Cyclase A/cGMP Signaling Pathway in the Kidney: Physiologic and Therapeutic Indications.International journal of molecular sciences · 2018Review
- Investigation of the role of nitric oxide/soluble guanylyl cyclase pathway in ascorbic acid-mediated protection against acute kidney injury in rats.Molecular and cellular biochemistry · 2015Article
- Increasing cGMP-dependent protein kinase activity attenuates unilateral ureteral obstruction-induced renal fibrosis.American journal of physiology. Renal physiology · 2014Article
- Article
- Increasing cGMP-dependent protein kinase I activity attenuates cisplatin-induced kidney injury through protection of mitochondria function.American journal of physiology. Renal physiology · 2013Article
- In situ transverse rectus abdominis myocutaneous flap: a rat model of myocutaneous ischemia reperfusion injury.Journal of visualized experiments : JoVE · 2013Article
- Transcriptional and post-transcriptional regulation of cGMP-dependent protein kinase (PKG-I): pathophysiological significance.Cardiovascular research · 2013Review
- Mouse model of ischemic acute kidney injury: technical notes and tricks.American journal of physiology. Renal physiology · 2012Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
cGMP-dependent protein kinase (PKG) is a multifunctional protein. Whether PKG plays a role in ischemia-reperfusion-induced kidney injury (IRI) is unknown. In this study, using an in vivo mouse model of renal IRI, we determined the effect of renal IRI on kidney PKG-I levels and also evaluated whether overexpression of PKG-I attenuates renal IRI. Our studies demonstrated that PKG-I levels (mRNA and protein) were significantly decreased in the kidney from mice undergoing renal IRI. Moreover, PKG-I transgenic mice had less renal IRI, showing improved renal function and less tubular damage compared with their wild-type littermates. Transgenic mice in the renal IRI group had decreased tubular cell apoptosis accompanied by decreased caspase 3 levels/activity and increased Bcl-2 and Bag-1 levels. In addition, transgenic mice undergoing renal IRI demonstrated reduced macrophage infiltration into the kidney and reduced production of inflammatory cytokines. In vitro studies showed that peritoneal macrophages isolated from transgenic mice had decreased migration compared with control macrophages. Taken together, these results suggest that PKG-I protects against renal IRI, at least in part through inhibiting inflammatory cell infiltration into the kidney, reducing kidney inflammation, and inhibiting tubular cell apoptosis.
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