ArticleJournal of the American Society of Nephrology : JASN2016
Renal 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase Is an Important Determinant of AKI Severity after Ischemia-Reperfusion.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Bacteriophages hijack 2',3'-cNMPs to enhance transposase-mediated phage DNA integration inScience advances · 2026Article
- Effects and Mechanism of 2'-AMP on Renal Vascular Resistance: Role of P2X1 Receptors.Journal of the American Society of Nephrology : JASN · 2026Article
- Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026Review
- Purine-based infochemicals and immunometabolites: a comparative review of emerging signaling pathways in plants and animals.FEMS microbiology reviews · 2025Review
- 8-Aminoguanine and its actions in the metabolic syndrome.Scientific reports · 2024Article
- Insights into the metabolism, signaling, and physiological effects of 2',3'-cyclic nucleotide monophosphates in bacteria.Critical reviews in biochemistry and molecular biology · 2023Review
- Mitochondria ROS and mitophagy in acute kidney injury.Autophagy · 2023Article
- Biochemical pathways of 8-aminoguanine production in Sprague-Dawley and Dahl salt-sensitive rats.Biochemical pharmacology · 2022Article
- CNPase, a 2',3'-Cyclic-nucleotide 3'-phosphodiesterase, as a Therapeutic Target to Attenuate Cardiac Hypertrophy by Enhancing Mitochondrial Energy Production.International journal of molecular sciences · 2021Article
- KIM-1-mediated anti-inflammatory activity is preserved by MUC1 induction in the proximal tubule during ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2021Article
- Long-Term Dipeptidyl Peptidase 4 Inhibition Worsens Hypertension and Renal and Cardiac Abnormalities in Obese Spontaneously Hypertensive Heart Failure Rats.Journal of the American Heart Association · 2021Article
- Alkaline Phosphatase Activity Is a Key Determinant of Vascular Responsiveness to Norepinephrine.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Targeting Mitochondria during Cold Storage to Maintain Proteasome Function and Improve Renal Outcome after Transplantation.International journal of molecular sciences · 2020Review
- Autophagy Function and Regulation in Kidney Disease.Biomolecules · 2020Review
- 2',3'-Cyclic-nucleotide 3'-phosphodiesterase contributes to epithelial-mesenchymal transition of lens epithelial cells through the notch signalling pathway.Cell proliferation · 2019Article
- 2',3'-cGMP exists in vivo and comprises a 2',3'-cGMP-guanosine pathway.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- SDF-1α (Stromal Cell-Derived Factor 1α) Induces Cardiac Fibroblasts, Renal Microvascular Smooth Muscle Cells, and Glomerular Mesangial Cells to Proliferate, Cause Hypertrophy, and Produce Collagen.Journal of the American Heart Association · 2017Article
- Novel roles for mucin 1 in the kidney.Current opinion in nephrology and hypertension · 2017Review
- ELABELA and an ELABELA Fragment Protect against AKI.Journal of the American Society of Nephrology : JASN · 2017Article
- Alkaline Phosphatase Inhibitors Attenuate Renovascular Responses to Norepinephrine.Hypertension (Dallas, Tex. : 1979) · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A positional isomer of 3',5'-cAMP, 2',3'-cAMP, is produced by kidneys in response to energy depletion, and renal 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) metabolizes 2',3'-cAMP to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimulate autophagy. Because autophagy protects against AKI, it is conceivable that inhibition of CNPase protects against ischemia-reperfusion (IR) -induced AKI. Therefore, we investigated renal outcomes, mitochondrial function, number, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice using a unique two-kidney, hanging-weight model of renal bilateral IR (20 minutes of ischemia followed by 48 hours of reperfusion). Analysis of urinary purines showed attenuated metabolism of 2',3'-cAMP to 2'-AMP in CNPase(-/-) mice. Neither genotype nor IR affected BP, heart rate, urine volume, or albumin excretion. In WT mice, renal IR reduced (14)C-inulin clearance (index of GFR) and increased renal vascular resistance (measured by transit time nanoprobes) and urinary excretion of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. IR did not affect these parameters in CNPase(-/-) mice. Histologic analysis revealed that IR induced severe damage in kidneys from WT mice, whereas histologic changes were minimal after IR in CNPase(-/-) mice. Measurements of renal cardiolipin levels, citrate synthase activity, rotenone-sensitive NADH oxidase activity, and proximal tubular mitochondrial and autophagosome area and number (by transmission electron microscopy) indicted accelerated autophagy/mitophagy in injured CNPase(-/-) mice. We conclude that CNPase deletion attenuates IR-induced AKI, in part by accelerating autophagy with targeted removal of damaged mitochondria.
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