Evidence mapPaperPMID 42548841Full record

ReviewFrontiers in neurology2026

High-altitude exposure and ischemic stroke: pathophysiological mechanisms and current perspectives.

Yuhuan Qiao, Yuding Luo, Yu Hu, Chuanxi Duan, Junhao Li, Xiaojing Luo, Jian Wang

Abstract readReview
In one paragraph

Review in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yuhuan Qiao *Department of Neurology, The Affiliated Hospital, Southwest Medical University, Luzhou, China.
Yuding Luo *Department of Neurology, Ya'an People's Hospital, Ya'an, China.
Yu HuDepartment of Neurology, The Affiliated Hospital, Southwest Medical University, Luzhou, China.
Chuanxi DuanDepartment of Neurology, Ya'an People's Hospital, Ya'an, China.
Junhao LiDepartment of Neurology, The Affiliated Hospital, Southwest Medical University, Luzhou, China.
Xiaojing LuoDepartment of Neurology, Ya'an People's Hospital, Ya'an, China.
Jian WangDepartment of Neurology, The Affiliated Hospital, Southwest Medical University, Luzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke remains the second leading cause of death worldwide and the third leading cause of disability-adjusted life year lost. In recent years, environmental and geographic determinants have been increasingly recognized as key contributors to stroke risk. High-altitude environments-characterized by chronic hypoxia, hypobaria, and elevated ultraviolet radiation-exert profound effects on cardiovascular and cerebrovascular physiology and substantially elevate stroke burden. A comprehensive understanding of how high altitude modulates the pathophysiology of ischemic stroke is therefore critical to optimizing prevention and tailored management in high-altitude populations. This narrative review synthesizes current evidence from peer-reviewed, English-language studies identified primarily through PubMed and supplemented by Google Scholar up to December 2025. We focus on three interrelated domains: physiological adaptation, maladaptive injury, and their implications on ischemic stroke under high-altitude conditions. Under mild-to-moderate hypoxic exposure, the human body achieves acclimatization via coordinated compensatory responses, including hematologic remodeling, enhanced ventilatory function, regulation of cerebral blood flow, and adaptive cardiac remodeling. With progressive increases in altitude or prolonged hypoxic exposure, however, these compensatory mechanisms become inadequate and shift toward maladaptation. This maladaptive transition is characterized by excessive erythropoiesis, heightened blood viscosity, hypercoagulability, endothelial dysfunction, blood-brain barrier disruption, amplified neuroinflammation, and oxidative stress. Collectively, these pathological cascades promote thrombogenesis and neuronal injury, thereby increasing susceptibility to ischemic stroke at high altitude. Future research priorities include the clarification of mechanisms governing the transition from physiological acclimatization to maladaptive injury, the identification of factors influencing individual responses to hypoxic exposure, the evaluation of targeted interventions capable of preserving beneficial adaptation or attenuating pathological processes, and the establishment of evidence-based prevention and management strategies for ischemic stroke in high-altitude populations.

Indexed as

acclimatizationhigh altitudehypoxiainflammationischemic strokeoxidative stress

Identifiers

PMID42548841
PMCPMC13429751

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.