ReviewCell regeneration (London, England)2025
Modulating mitochondrial metabolism: a neuroprotective mechanism for hypoxic-ischemic preconditioning.
Review in Cell regeneration (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed.
- Cyclic Altitude Training, Mitochondrial Health, and the Oral-Airway Axis: Intermittent Hypoxia Between Adaptation and Disease.Journal of clinical medicine · 2026Review
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- Progress of Research on Cognitive Impairment in Patients With Chronic Obstructive Pulmonary Disease.Actas espanolas de psiquiatria · 2026Review
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Hypoxia-ischemia plays a role in the physiological and pathological processes of various diseases and presents a common challenge for humans under extreme environmental conditions. Neurons are particularly sensitive to hypoxia-ischemia, and prolonged exposure may lead to irreversible brain damage. The primary mechanisms underlying this damage include energy depletion, mitochondrial dysfunction, oxidative stress, inflammation, and apoptosis. Mitochondria serve as primary organelles for adenosine triphosphate (ATP) production, and mitochondrial dysfunction plays a crucial role in mediating hypoxic pathophysiological processes. Hypoxic-ischemic preconditioning (H/IPC) is an endogenous cellular protective mechanism that reduces the damage caused by lethal hypoxic stressors. In this review, we summarize the potential role of H/IPC and its protective effects on mitochondrial quality control and function. This perspective offers a new approach for treating diseases caused by hypoxia-ischemia.
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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.