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病毒感染所致生精功能障碍的可能机制:来自新冠病毒病的见解

Possible mechanisms of spermatogenic dysfunction induced by viral infections: Insights from COVID-19.

作者信息

Okada Keisuke, Kin Chanhyon, Yamashita Yosuke, Kawamura Shun, Sato Katsuya, Chiba Koji, Miyake Hideaki

机构信息

Department of Urology Kobe City Medical Center West Hospital Kobe Japan.

Division of Urology, Department of Organs Therapeutics Kobe University Graduate School of Medicine Kobe Japan.

出版信息

Reprod Med Biol. 2025 Jan 22;24(1):e12625. doi: 10.1002/rmb2.12625. eCollection 2025 Jan-Dec.

DOI:10.1002/rmb2.12625
PMID:39845480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11751869/
Abstract

BACKGROUND

As the COVID-19 pandemic nears resolution in 2024, the mechanisms by which SARS-CoV-2 and other viral infections induce spermatogenic dysfunction remain poorly understood. This review examines the mechanisms by which viral infections, particularly COVID-19, disrupt spermatogenesis and highlights the implications for male reproductive health. While reports suggest that spermatogenic dysfunction caused by COVID-19 is mild and transient, these findings may have broader applications in understanding and treating spermatogenic dysfunction caused by future viral infections.

METHODS

The PubMed database was searched to identify original and review articles investigating the mechanisms by which viral infections, particularly SARS-CoV-2, contribute to spermatogenic dysfunction.

MAIN FINDINGS

SARS-CoV-2 affects the testis through multiple mechanisms, including ACE2 receptor-mediated entry, direct viral damage, inflammatory response, blood-testis barrier disruption, hormonal imbalance, oxidative stress, and impaired spermatogenesis. The combination of these factors can disrupt testicular function and highlights the complexity of the effects of COVID-19 on male reproductive health.

CONCLUSION

COVID-19 may disrupt spermatogenesis through direct testicular infection, systemic inflammation, hormonal disruption, and oxidative stress. Ongoing research, vaccination efforts, and clinical vigilance are essential to address these challenges and develop effective treatment and prevention strategies.

摘要

背景

随着2024年新冠疫情接近尾声,严重急性呼吸综合征冠状病毒2(SARS-CoV-2)及其他病毒感染诱发生精功能障碍的机制仍未完全明了。本综述探讨病毒感染,尤其是新冠病毒感染,破坏生精过程的机制,并强调其对男性生殖健康的影响。虽然有报告表明新冠病毒引起的生精功能障碍是轻微且短暂的,但这些发现可能在理解和治疗未来病毒感染导致的生精功能障碍方面具有更广泛的应用。

方法

检索PubMed数据库,以确定研究病毒感染,特别是SARS-CoV-2导致生精功能障碍机制的原创性文章和综述。

主要发现

SARS-CoV-2通过多种机制影响睾丸,包括血管紧张素转换酶2(ACE2)受体介导的进入、直接病毒损伤、炎症反应、血睾屏障破坏、激素失衡、氧化应激和生精受损。这些因素的综合作用可破坏睾丸功能,并凸显了新冠病毒对男性生殖健康影响的复杂性。

结论

新冠病毒可能通过直接睾丸感染、全身炎症、激素紊乱和氧化应激破坏生精过程。持续的研究、疫苗接种工作和临床警惕对于应对这些挑战以及制定有效的治疗和预防策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d0b/11751869/85677cf0aefa/RMB2-24-e12625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d0b/11751869/85677cf0aefa/RMB2-24-e12625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d0b/11751869/85677cf0aefa/RMB2-24-e12625-g002.jpg

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本文引用的文献

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