ArticleScientific reports2025
Rapamycin alleviates hypothalamic injury in exertional heat stroke rats by activating mitophagy through the mTOR/Pink1/Parkin pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- PINK1/Parkin-Mediated Mitophagy Participates in High-Altitude Hypoxia Adaptation in Yaks via Energy Metabolism Remodeling.Animals : an open access journal from MDPI · 2026Article
- Coordinated Bone-Muscle Axis Association in South China Carp (Foods (Basel, Switzerland) · 2026Article
- Energy metabolic dysregulation in heat stroke: from mitochondrial dysfunction to multi-organ failure mechanisms and targeted intervention.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exertional heat stroke (EHS) causes severe central nervous system damage, with mitochondrial dysfunction and oxidative stress playing major roles. Mitophagy, regulated by the Pink1/Parkin pathway, removes damaged mitochondria. Here, we investigated the potential of rapamycin (RAPA) to reduce hypothalamic injury in rats subjected to EHS. Forty healthy male Sprague-Dawley rats were randomly assigned to control, RAPA, EHS, and EHS + RAPA groups (10 rats each). Core temperatures were measured, and survival curves were generated. Hypothalamic tissue underwent hematoxylin-eosin and Nissl staining for histopathological assessment. Hypothalamic mitochondrial membrane potential, reactive oxygen species (ROS), and malonaldehyde (MDA) levels were measured. Western blotting assessed mammalian target of RAPA (mTOR), phosphorylated mTOR, Pink1, Parkin, P62, and microtubule-associated protein 1 Light chain 3 (LC3) expression, and calculated the LC3II/LC3I ratio. Immunofluorescence evaluated Pink1-Parkin and LC3-Tom20 co-localization in hypothalamic tissue. EHS and EHS + RAPA groups showed markedly increased core temperatures. RAPA mitigated pathological injury and apoptosis, reduced ROS and MDA levels, and enhanced mitochondrial membrane potential. It downregulated mTOR and p62 levels, upregulated Pink1 and Parkin, increased LC3II/LC3I ratio, and promoted LC3-Tom20 and Pink1-Parkin interactions in the hypothalamic tissue of rats treated with EHS, thereby alleviating hypothalamic injury and preserving hypothalamic function.
Indexed as
Identifiers
What OpenQuestion holds
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.