详细信息
High-altitude hypoxia and male reproductive dysfunction: testicular oxygen homeostasis, microenvironmental injury and spermatogonial niche vulnerability ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:High-altitude hypoxia and male reproductive dysfunction: testicular oxygen homeostasis, microenvironmental injury and spermatogonial niche vulnerability
作者:Li, Jiahao[1,2,3];Meng, Dongdong[2];Zhang, Bin[2,4];Yang, Changfeng[1];Ma, Fulin[1];Li, Forong[1];Wang, Yanbao[2];Zheng, Zhaoyang[2];Wang, Zhanzhong[2];Li, Mengkun[2];Liu, Lingqi[2];Chang, Dehui[1,2]
第一作者:Li, Jiahao
通信作者:Chang, DH[1];Chang, DH[2]
机构:[1]Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Peoples R China;[2]940th Hosp Joint Logist Support Force Chinese Peop, Dept Urol, Lanzhou, Peoples R China;[3]Gansu Prov Key Lab Stem Cells & Gene Drugs, Lanzhou, Peoples R China;[4]Northwest Minzu Univ, Lanzhou, Peoples R China
第一机构:甘肃中医药大学
通信机构:[1]corresponding author), Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou, Peoples R China;[2]corresponding author), 940th Hosp Joint Logist Support Force Chinese Peop, Dept Urol, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;
年份:2026
卷号:17
外文期刊名:FRONTIERS IN ENDOCRINOLOGY
收录:;Scopus(收录号:2-s2.0-105051421365);WOS:【SCI-EXPANDED(收录号:WOS:001879716400001)】;
基金:The author(s) declared that financial support was received for this work and/or its publication. This work was supported by the Central University Scientific Research Project of Northwest Minzu University (No. 31920260109, No. 31920240072); Natural Science Foundation of Gansu Province (No. 23JRRA531, No. 23JRRA001); Key University Collaborative Innovation Project of Gansu University of Chinese Medicine (No. HXLH-XTCX11); Science and Technology Project of Lanzhou City (No. 2023-2-63). The funders had no role in the design of the study, data collection, analysis, decision to publish, or preparation of the manuscript.
语种:英文
外文关键词:blood-testis barrier; high-altitude hypoxia; hypobaric hypoxia; male reproduction; reproductive endocrinology; spermatogonial stem cells; testicular microenvironment; testicular oxygen homeostasis
摘要:High-altitude hypoxia is a sustained environmental stressor that reduces inspired oxygen pressure and challenges tissue oxygen delivery. The male reproductive system is sensitive to oxygen availability, vascular perfusion, testosterone support, Sertoli-cell metabolic function and blood-testis barrier integrity. Human high-altitude exposure studies, mountaineering observations and animal hypobaric hypoxia models indicate that exposure to high altitude or hypobaric hypoxia is associated with reductions in sperm concentration, total sperm count, motility, viability and normal morphology, accompanied in experimental models by testicular structural injury, oxidative stress and reproductive endocrine alterations. However, the magnitude and reversibility of these changes vary substantially across studies. This variability suggests that altitude-related reproductive dysfunction is not a single linear consequence of hypoxia, but a dynamic process governed by exposure intensity, duration, acclimatization, systemic stressors and local testicular compensatory capacity. Building on the classical hypoxia-oxidative stress-germ-cell injury paradigm, this review proposes an integrated framework centered on testicular oxygen homeostasis, dual microenvironmental injury and spermatogonial niche vulnerability. In this model, high-altitude hypoxia first challenges the balance among oxygen delivery, microvascular blood flow, temperature and metabolism. When compensation fails, injury is propagated through two interconnected compartments: the interstitial vascular endothelial niche-Leydig-cell-immune axis and the seminiferous Sertoli-cell-blood-testis barrier-germ-cell support system. Peritubular myoid cells, the basement membrane and extracellular matrix form a boundary layer that links these compartments and participates in the spermatogonial stem-cell niche. The rete testis/efferent ductules, epididymal segmental microenvironment, blood-epididymis barrier and seminal extracellular vesicles are best interpreted as downstream or modifying layers rather than primary mechanisms. Whether injury reaches spermatogonia or the spermatogonial stem-cell niche may determine whether recovery is rapid and complete or delayed and incomplete. The review also identifies evidence gaps, including direct measurement of local testicular oxygen tension, compartment-specific experimental designs, niche-targeted endpoints and longitudinal high-altitude/lowland return cohorts.
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