ArticleAmerican journal of physiology. Renal physiology2016
Proximal tubule-targeted heme oxygenase-1 in cisplatin-induced acute kidney injury.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 70 citations in OpenAlex.
- Tanshinone IIA attenuates psoriasis via Nrf2/HO-1 activation: Mechanistic insights from preclinical models.Biochemistry and biophysics reports · 2026Article
- Loss of proximal tubule lactate dehydrogenase A exacerbates nephrotoxic acute kidney injury through metabolic dysregulation.American journal of physiology. Renal physiology · 2026Article
- Naringenin-functionalized polyester nanoparticles improve oral urolithin A delivery and protect against cisplatin-induced kidney injury via heme oxygenase-1 activation and mitochondrial quality control.The Journal of pharmacology and experimental therapeutics · 2026Article
- Reduction of Vancomycin-Associated Acute Kidney Injury With Montelukast.The Journal of infectious diseases · 2025Article
- Morin hydrate protects against cisplatin-induced testicular toxicity by modulating ferroptosis and steroidogenesis genes' expression and upregulating Nrf2/Heme oxygenase-1.Scientific reports · 2025Article
- Article
- Protective roles of thrombomodulin in cisplatin-induced nephrotoxicity through the inhibition of oxidative and endoplasmic reticulum stress.Scientific reports · 2024Article
- Targeted expression of heme oxygenase-1 in satellite cells improves skeletal muscle pathology in dystrophic mice.Skeletal muscle · 2024Article
- Redox Regulation of Nrf2 in Cisplatin-Induced Kidney Injury.Antioxidants (Basel, Switzerland) · 2023Review
- Identification of Cytoprotective Small-Molecule Inducers of Heme-Oxygenase-1.Antioxidants (Basel, Switzerland) · 2022Article
- Renal hypoxia-HIF-PHD-EPO signaling in transition metal nephrotoxicity: friend or foe?Archives of toxicology · 2022Review
- Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion.Science advances · 2022Article
- Kidney tubule iron loading in experimental focal segmental glomerulosclerosis.Scientific reports · 2022Article
- Functional consequence of myeloid ferritin heavy chain on acute and chronic effects of rhabdomyolysis-induced kidney injury.Frontiers in medicine · 2022Article
- VEGFR3 tyrosine kinase inhibition aggravates cisplatin nephrotoxicity.American journal of physiology. Renal physiology · 2021Article
- IFT88 deficiency in proximal tubular cells exaggerates cisplatin-induced injury by suppressing autophagy.American journal of physiology. Renal physiology · 2021Article
- Adapting decarbonylation chemistry for the development of prodrugs capable ofChemical science · 2021Article
- Heme Burden and Ensuing Mechanisms That Protect the Kidney: Insights from Bench and Bedside.International journal of molecular sciences · 2021Review
- UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021Review
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that catalyzes the breakdown of heme to biliverdin, carbon monoxide, and iron. The beneficial effects of HO-1 expression are not merely due to degradation of the pro-oxidant heme but are also credited to the by-products that have potent, protective effects, including antioxidant, anti-inflammatory, and prosurvival properties. This is well reflected in the preclinical animal models of injury in both renal and nonrenal settings. However, excessive accumulation of the by-products can be deleterious and lead to mitochondrial toxicity and oxidative stress. Therefore, use of the HO system in alleviating injury merits a targeted approach. Based on the higher susceptibility of the proximal tubule segment of the nephron to injury, we generated transgenic mice using cre-lox technology to enable manipulation of HO-1 (deletion or overexpression) in a cell-specific manner. We demonstrate the validity and feasibility of these mice by breeding them with proximal tubule-specific Cre transgenic mice. Similar to previous reports using chemical modulators and global transgenic mice, we demonstrate that whereas deletion of HO-1, specifically in the proximal tubules, aggravates structural and functional damage during cisplatin nephrotoxicity, selective overexpression of HO-1 in proximal tubules is protective. At the cellular level, cleaved caspase-3 expression, a marker of apoptosis, and p38 signaling were modulated by HO-1. Use of these transgenic mice will aid in the evaluation of the effects of cell-specific HO-1 expression in response to injury and assist in the generation of targeted approaches that will enhance recovery with reduced, unwarranted adverse effects.
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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.