Endothelial dysfunction in autoimmune, pulmonary, and kidney systems, and exercise tolerance following SARS-CoV-2 infection.

Endothelial dysfunction in autoimmune, pulmonary, and kidney systems, and exercise tolerance following SARS-CoV-2 infection.
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SARS-CoV-2感染后自身免疫、肺和肾系统的内皮功能障碍与运动耐量

DOI:
10.3389/fmed.2023.1197061
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发表时间:
2023
影响因子:
3.9
通讯作者:
--
中科院分区:
医学3区
文献类型:
--
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长冠状病毒病的特征是严重急性呼吸综合征冠状病毒-2 (SARS-CoV-2)感染超过3个月的持续症状,持续至少2个月,并且无法用其他诊断来解释。自主神经系统、免疫系统、内皮系统和高凝可能是COVID症状延长的机制。尽管认识到长期COVID带来的公共卫生挑战,但目前对病理生理基础的理解仍在不断发展。在这篇叙述性综述中,我们探讨了SARS-CoV-2感染对T细胞激活的长期影响,如自身免疫性疾病和内皮细胞功能障碍,涉及肺和肾结构内的血管损伤。我们已经描述了内皮功能障碍和血管异常如何通过外周氧提取受损来强调长COVID患者运动不耐受的发现。
Long COVID is characterized by persistent symptoms beyond 3-months of severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) infection that last for at least 2 months and cannot be explained by an alternative diagnosis. Autonomic, immunologic, endothelial, and hypercoagulation are implicated as possible mechanisms of long COVID symptoms. Despite recognition of the public health challenges posed by long COVID, the current understanding of the pathophysiological underpinnings is still evolving. In this narrative review, we explore the long-term effects of SARS-CoV-2 infection on T cell activation such as autoimmune disorders and endothelial cell dysfunction involving vascular impairments within pulmonary and renal architecture. We have described how endothelial dysfunction and vascular abnormalities may underscore findings of exercise intolerance by way of impaired peripheral oxygen extraction in individuals with long COVID.
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