ArticleJCI insight2020
Selective inhibition of arginase-2 in endothelial cells but not proximal tubules reduces renal fibrosis.
Article in JCI insight, 2020. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Endothelial Ffar4 protects against diabetic kidney disease by potentiating endogenous retinoic acid metabolism.Cellular & molecular biology letters · 2026Article
- The Janus face of L-arginine supplementation in cardiovascular health and aging exploration of underlying mechanisms.Frontiers in aging · 2026Review
- Research dynamics and drug treatment of renal fibrosis from a mitochondrial perspective: a historical text data analysis based on bibliometrics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Macula densa nitric oxide synthase 1β restoration by kidney alkalization enhances renal graft outcomes.American journal of physiology. Renal physiology · 2025Article
- Deficiency of Growth Arrest and DNA Damage-Inducible 45 α -R-Loop Pathway and Kidney Injury in Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2025Article
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- Endothelial CXCR2 deficiency attenuates renal inflammation and glycocalyx shedding through NF-κB signaling in diabetic kidney disease.Cell communication and signaling : CCS · 2024Article
- Acyloxyacyl Hydrolase Protects against Kidney Injury via Inhibition of Tubular CD74-Macrophage Crosstalk.International journal of biological sciences · 2024Article
- From Physiology to Pathology: The Role of Mitochondria in Acute Kidney Injuries and Chronic Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Elevation of Arginase-II in Podocytes Contributes to Age-Associated Albuminuria in Male Mice.International journal of molecular sciences · 2023Article
- Molecular Targets of Brown Algae Phlorotannins for the Therapy of Inflammatory Processes of Various Origins.Marine drugs · 2022Review
- Roles of SIRT6 in kidney disease: a novel therapeutic target.Cellular and molecular life sciences : CMLS · 2021Article
- 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
- PGC1α is required for the renoprotective effect of lncRNA Tug1 in vivo and links Tug1 with urea cycle metabolites.Cell reports · 2021Article
- The CAT-1 is out of the bag: endothelial Cationic Amino Acid Transporter-1 is a critical player in cardiorenal syndrome type 2.Clinical science (London, England : 1979) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fibrosis is the final common pathway in the pathophysiology of most forms of chronic kidney disease (CKD). As treatment of renal fibrosis still remains largely supportive, a refined understanding of the cellular and molecular mechanisms of kidney fibrosis and the development of novel compounds are urgently needed. Whether arginases play a role in the development of fibrosis in CKD is unclear. We hypothesized that endothelial arginase-2 (Arg2) promotes the development of kidney fibrosis induced by unilateral ureteral obstruction (UUO). Arg2 expression and arginase activity significantly increased following renal fibrosis. Pharmacologic blockade or genetic deficiency of Arg2 conferred kidney protection following renal fibrosis, as reflected by a reduction in kidney interstitial fibrosis and fibrotic markers. Selective deletion of Arg2 in endothelial cells (Tie2Cre/Arg2fl/fl) reduced the level of fibrosis after UUO. In contrast, selective deletion of Arg2 specifically in proximal tubular cells (Ggt1Cre/Arg2fl/fl) failed to reduce renal fibrosis after UUO. Furthermore, arginase inhibition restored kidney nitric oxide (NO) levels, oxidative stress, and mitochondrial function following UUO. These findings indicate that endothelial Arg2 plays a major role in renal fibrosis via its action on NO and mitochondrial function. Blocking Arg2 activity or expression could be a novel therapeutic approach for prevention of CKD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.