ArticleClinical and experimental nephrology2019
22-oxacalcitriol prevents acute kidney injury via inhibition of apoptosis and enhancement of autophagy.
Article in Clinical and experimental nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Vitamin D and Acute Kidney Injury: A Two-Way Causality Relation and a Predictive, Prognostic, and Therapeutic Role of Vitamin D.Frontiers in nutrition · 2020Pooled it
- The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025Review
- Vitamin D metabolism in critically ill patients with acute kidney injury: a prospective observational study.Critical care (London, England) · 2024Observational
- Autophagy in renal fibrosis: Protection or promotion?Frontiers in pharmacology · 2022Review
- Autophagy and Inflammation Regulation in Acute Kidney Injury.Frontiers in physiology · 2020Review
- Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation.Yonsei medical journal · 2019Article
- Sirt3 suppresses calcium oxalate-induced renal tubular epithelial cell injury via modification of FoxO3a-mediated autophagy.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pathophysiology of ischemic acute kidney injury (AKI) is thought to include a complex interplay between tubular cell damage and regeneration. Several lines of evidences suggest a potential renoprotective effect of vitamin D. In this study, we investigated the effect of 22-oxacalcitriol (OCT), a synthetic vitamin D analogue, on renal fate in a rat model of ischemia reperfusion injury (IRI) induced acute kidney injury (AKI).
methods22-oxacalcitriol (OCT) was administered via intraperitoneal (IP) injection before ischemia, and continued after IRI that was performed through bilateral clamping of the renal pedicles. 96 h after reperfusion, rats were sacrificed for the evaluation of autophagy, apoptosis, and cell cycle arrest. Additionally, assessments of toll-like receptors (TLR), interferon gamma (IFN-g) and sodium-hydrogen exchanger-1 (NHE-1) were also performed to examine their relations to OCT-mediated cell response.
resultsTreatment with OCT-attenuated functional deterioration and histological damage in IRI induced AKI, and significantly decreased cell apoptosis and fibrosis. In comparison with IRI rats, OCT + IRI rats manifested a significant exacerbation of autophagy as well as reduced cell cycle arrest. Moreover, the administration of OCT decreased IRI-induced upregulation of TLR4, IFN-g and NHE-1.
conclusionThese results demonstrate that treatment with OCT has a renoprotective effect in ischemic AKI, possibly by suppressing cell loss. Changes in the expression of IFN-g and NHE-1 could partially link OCT to the cell survival-promoted effects.
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