ArticleCell2025
HypoxyStat, a small-molecule form of hypoxia therapy that increases oxygen-hemoglobin affinity.
Article in Cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed.
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- Hypoxia rescues complex 1-associated disease caused by proteostatic defects.Nature metabolism · 2026Article
- Oxygen relief for a proteostasis-driven disease associated with mitochondrial complex I dysfunction.Nature metabolism · 2026Article
- Soft Hypoxia-Adaptive Bioelectronics Integrating PEDOT:PSS/Polydopamine/Enzyme Biocomposites for Closed-Loop Therapeutics of Chronic Wounds.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Disease Gene THAP12 is a Transcriptional Regulator of Mitochondrial ETC Complex I.bioRxiv : the preprint server for biology · 2026Article
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- Exercise and smoking: health rivals revealing shared protective mechanisms in Parkinson's?NPJ Parkinson's disease · 2026Review
- Hypoxia-induced autophagic degradation of HIF-1α attenuates cellular aging and extends mammalian lifespan.Nature aging · 2026Article
- Pluripotent stem-cell-based screening uncovers sildenafil as a mitochondrial disease therapy.Cell · 2026Article
- Red blood cells serve as a primary glucose sink to improve glucose tolerance at altitude.Cell metabolism · 2026Article
- Impaired Complex I dysregulates neural/glial precursors and corpus callosum development revealing postnatal defects in Leigh syndrome mice.EMBO molecular medicine · 2026Article
- Hemoglobin and human longevity: integrating oxygen transport, redox biology, and aging pathways - a narrative review.Annals of medicine and surgery (2012) · 2026Review
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Hypoxia, Psychedelics, and Terminal Lucidity: A Perspective on Neuroplasticity and Neuropsychiatric Disorders.ACS pharmacology & translational science · 2025Review
- Developing a novel aging assessment model to uncover heterogeneity in organ aging and screening of aging-related drugs.Genome medicine · 2025Article
- Advances in Therapeutics for Chronic Lung Diseases: From Standard Therapies to Emerging Breakthroughs.Journal of clinical medicine · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
We have previously demonstrated that chronic inhaled hypoxia is remarkably therapeutic in the premier animal model of mitochondrial Leigh syndrome, the Ndufs4 knockout (KO) mouse. Subsequent work has extended this finding to additional mitochondrial diseases and more common conditions. However, challenges inherent to gas-based therapies have hindered the rapid translation of our findings to the clinic. Here, we tested a small molecule (hereafter termed HypoxyStat) that increases the binding affinity of hemoglobin for oxygen, thereby decreasing oxygen offloading to tissues. Daily oral dosing of HypoxyStat caused systemic hypoxia in mice breathing normoxic (21% O
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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.