Omolaoye Temidayo S, Jalaleddine Nour, Cardona Maya Walter D, du Plessis Stefan S
Department of Basic Sciences, College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai, United Arab Emirates.
Reproduction Group, Department of Microbiology and Parasitology, Faculty of Medicine, Universidad de Antioquia, Medellin, Colombia.
Front Physiol. 2022 May 23;13:866675. doi: 10.3389/fphys.2022.866675. eCollection 2022.
The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on male infertility has lately received significant attention. SARS-CoV-2, the virus that causes coronavirus disease (COVID-19) in humans, has been shown to impose adverse effects on both the structural components and function of the testis, which potentially impact spermatogenesis. These adverse effects are partially explained by fever, systemic inflammation, oxidative stress, and an increased immune response leading to impaired blood-testis barrier. It has been well established that efficient cellular communication gap junctions or functional channels is required for tissue homeostasis. Connexins and pannexins are two protein families that mediate autocrine and paracrine signaling between the cells and the extracellular environment. These channel-forming proteins have been shown to play a role in coordinating cellular communication in the testis and epididymis. Despite their role in maintaining a proper male reproductive milieu, their function is disrupted under pathological conditions. The involvement of these channels has been well documented in several physiological and pathological conditions and their designated function in infectious diseases. However, their role in COVID-19 and their meaningful contribution to male infertility remains to be elucidated. Therefore, this review highlights the multivariate pathophysiological mechanisms of SARS-CoV-2 involvement in male reproduction. It also aims to shed light on the role of connexin and pannexin channels in disease progression, emphasizing their unexplored role and regulation of SARS-CoV-2 pathophysiology. Finally, we hypothesize the possible involvement of connexins and pannexins in SARS-CoV-2 inducing male infertility to assist future research ideas targeting therapeutic approaches.
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）对男性不育的影响近来受到了广泛关注。SARS-CoV-2是导致人类冠状病毒病（COVID-19）的病毒，已被证明会对睾丸的结构成分和功能产生不利影响，这可能会影响精子发生。这些不利影响部分可归因于发热、全身炎症、氧化应激以及免疫反应增强导致血睾屏障受损。众所周知，有效的细胞通讯——间隙连接或功能性通道——对于组织稳态是必需的。连接蛋白和泛连接蛋白是两个蛋白质家族，它们介导细胞与细胞外环境之间的自分泌和旁分泌信号传导。这些形成通道的蛋白质已被证明在协调睾丸和附睾中的细胞通讯中发挥作用。尽管它们在维持适当的男性生殖环境中发挥作用，但在病理条件下其功能会受到破坏。这些通道在几种生理和病理状况及其在传染病中的特定功能中的参与已有充分记录。然而，它们在COVID-19中的作用及其对男性不育的重要贡献仍有待阐明。因此，本综述强调了SARS-CoV-2参与男性生殖的多因素病理生理机制。它还旨在阐明连接蛋白和泛连接蛋白通道在疾病进展中的作用，强调它们在SARS-CoV-2病理生理学中未被探索的作用和调节。最后，我们推测连接蛋白和泛连接蛋白可能参与SARS-CoV-2诱导男性不育，以协助未来针对治疗方法的研究思路。
