ArticleEnvironment & health (Washington, D.C.)2024
Extreme Heat Exposure Induced Acute Kidney Injury through NLRP3 Inflammasome Activation in Mice.
Article in Environment & health (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Disparity in the regulation and prevention of water versus sodium imbalance in heat-stress nephropathy: a phylogenetic perspective.Clinical kidney journal · 2026Review
- Microvesicle release drives cycles of mitophagy flux disruption and inflammatory amplification in sepsis-induced myocardial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rising Global Temperatures and Kidney Health: A Comprehensive Review of Current Evidence.Life (Basel, Switzerland) · 2025Review
- One day of environment-induced heat stress causes injury to the murine kidney.Experimental physiology · 2025Article
- Eicosapentaenoic Acid and Urolithin a Synergistically Mitigate Heat Stroke-Induced NLRP3 Inflammasome Activation in Microglial Cells.Nutrients · 2025Article
- Association between heatwave exposure and rapid kidney function decline: a longitudinal cohort study from CHARLS.BMC public health · 2025Article
- Wearable microfluidic biosensors with haptic feedback for continuous monitoring of hydration biomarkers in workers.NPJ digital medicine · 2025Article
- Surface frustrated Lewis pairs in titanium nitride enable gas phase heterogeneous CONature communications · 2024Article
- Vitamin D protects spermatogonia and Sertoli cells from heat stress damage by inhibiting NLRP3.Frontiers in pediatrics · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Climate change has resulted in a marked increase in heat extremes that carry a severe risk for morbidity and mortality. Kidney is sensitive to heat stimulation, and acute kidney injury (AKI) is the early event. In this study, we investigated the adverse effects of heat extremes and their underlying mechanism. A total of 16 wild-type C57BL/6N mice were randomly divided into groups of control (exposed to 22 ± 0.5 °C) and heat (exposed to 39.5 ± 0.5 °C until the core body temperature reached the maximum). First, extreme heat exposure induced AKI evidenced by kidney dysfunction and morphological impairment. In addition, heat exposure suppressed expression of molecules for mitochondrial energetics and fatty acid beta-oxidation and disturbed the balance of oxidative stress in the kidney. Moreover, heat exposure enhanced the protein levels in the upstream signaling pathway for NLRP3 inflammasome formation, followed by NLRP3 inflammasome activation and inflammatory cytokine production. These findings demonstrated that acute extreme heat exposure may induce AKI through the NLRP3 inflammasome formation and activation.
Identifiers
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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.