ArticlePloS one2014
Role of TRPV1 channels in ischemia/reperfusion-induced acute kidney injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Deletion of the TRPV1 channel attenuates afferent renal nerve responses to renal artery occlusion but not elevated renal pelvic pressure.The Journal of physiology · 2026Article
- Spice Up Your Kidney: A Review on the Effects of Capsaicin in Renal Physiology and Disease.International journal of molecular sciences · 2024Review
- Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress.BMC molecular and cell biology · 2023Article
- The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury.Cell death discovery · 2022Review
- Role of TRPC6 in kidney damage after acute ischemic kidney injury.Scientific reports · 2022Article
- Transient receptor potential vanilloid subtype 1: A potential therapeutic target for fibrotic diseases.Frontiers in physiology · 2022Review
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- Endocannabinoid System in Polycystic Kidney Disease.American journal of nephrology · 2022Article
- NLRP3 associated with chronic kidney disease progression after ischemia/reperfusion-induced acute kidney injury.Cell death discovery · 2021Article
- Renal Tubular Epithelial TRPA1 Acts as An Oxidative Stress Sensor to Mediate Ischemia-Reperfusion-Induced Kidney Injury through MAPKs/NF-κB Signaling.International journal of molecular sciences · 2021Article
- Targeting TRPV1-mediated autophagy attenuates nitrogen mustard-induced dermal toxicity.Signal transduction and targeted therapy · 2021Article
- Cannabinoid Receptor 1 Inhibition in Chronic Kidney Disease: A New Therapeutic Toolbox.Frontiers in endocrinology · 2021Review
- Short-Term Diet Restriction but Not Alternate Day Fasting Prevents Cisplatin-Induced Nephrotoxicity in Mice.Biomedicines · 2020Article
- Assessment of Pharmacology, Safety, and Metabolic activity of Capsaicin Feeding in Mice.Scientific reports · 2019Article
- Risks of Impaired Organ Protection with Inhibiting Transient Receptor Potential Vanilloid 1.Anesthesiology · 2018Article
- Transient Receptor Potential Vanilloid 4 Channel Deficiency Aggravates Tubular Damage after Acute Renal Ischaemia Reperfusion.Scientific reports · 2018Article
- Non-opioid analgesic use and concerns for impaired organ protection.British journal of anaesthesia · 2018Article
- Decreased expression of TRPV1 in renal cell carcinoma: association with tumor Fuhrman grades and histopathological subtypes.Cancer management and research · 2018Article
- Transient receptor potential vanilloid 1 inhibitors block laparotomy- and opioid-induced infarct size reduction in rats.British journal of pharmacology · 2017Article
- Endotoxemia induces lung-brain coupling and multi-organ injury following cerebral ischemia-reperfusion.Experimental neurology · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTransient receptor potential vanilloid 1 (TRPV1) -positive sensory nerves are widely distributed in the kidney, suggesting that TRPV1-mediated action may participate in the regulation of renal function under pathophysiological conditions. Stimulation of TRPV1 channels protects against ischemia/reperfusion (I/R)-induced acute kidney injury (AKI). However, it is unknown whether inhibition of these channels is detrimental in AKI or not. We tested the role of TRPV1 channels in I/R-induced AKI by modulating these channels with capsaicin (TRPV1 agonist), capsazepine (TRPV1 antagonist) and using Trpv1-/- mice. METHODS AND
resultsAnesthetized C57BL/6 mice were subjected to 25 min of renal ischemia and 24 hrs of reperfusion. Mice were pretreated with capsaicin (0.3 mg/kg body weight) or capsazepine (50 mg/kg body weight). Capsaicin ameliorated the outcome of AKI, as measured by serum creatinine levels, tubular damage,neutrophil gelatinase-associated lipocalin (NGAL) abundance and Ly-6B.2 positive polymorphonuclear inflammatory cells in injured kidneys. Neither capsazepine nor deficiency of TRPV1 did deteriorate renal function or histology after AKI. Measurements of endovanilloids in kidney tissue indicate that 20-hydroxyeicosatetraeonic acid (20-HETE) or epoxyeicosatrienoic acids (EETs) are unlikely involved in the beneficial effects of capsaicin on I/R-induced AKI.
conclusionsActivation of TRPV1 channels ameliorates I/R-induced AKI, but inhibition of these channels does not affect the outcome of AKI. Our results may have clinical implications for long-term safety of renal denervation to treat resistant hypertension in man, with respect to the function of primary sensory nerves in the response of the kidney to ischemic stimuli.
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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.