将 COVID-19 与癌症联系起来:基本机制

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Sourabh Tyagi , Nipanshi Tyagi , Anu Singh , Akanksha Gautam , Awantika Singh , Shelja Jindal , Rana P. Singh , Rupesh Chaturvedi , Hemant Ritturaj Kushwaha
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引用次数: 0

摘要

由严重急性呼吸系统综合症冠状病毒 2(SARS-CoV-2)引起的 COVID-19 引发了一场全球性的健康危机,其临床表现多种多样。在患有其他疾病的患者中发现了可能易受 SARS-CoV-2 感染的人群。有趣的是,COVID-19 与癌症在病理生理学层面存在相似之处,这表明两者之间可能存在联系。本综述将讨论 COVID-19 与癌症之间所有可能的关联。血管紧张素转换酶 2 (ACE2) 和跨膜丝氨酸蛋白酶 2 (TMPRSS2) 等受体的表达会增加 COVID-19 的易感性。SARS-CoV-2 感染可能会通过细胞因子风暴、组织缺氧、T 细胞反应受损、自噬、中性粒细胞活化和氧化应激等机制增加癌症易感性并加速癌症进展。这些机制共同导致了肿瘤微环境中的免疫抑制、细胞凋亡受阻和细胞信号改变,为肿瘤生长、转移和复发创造了有利条件。此外,还介绍了已获批准的疫苗及其对癌症患者的影响以及新的临床试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Linking COVID-19 and cancer: Underlying mechanism
COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), lead to a global health crisis with a spectrum of clinical manifestations. A potentially vulnerable category for SARS-CoV-2 infection was identified in patients with other medical conditions. Intriguingly, parallels exist between COVID-19 and cancer at the pathophysiological level, suggesting a possible connection between them. This review discusses all possible associations between COVID-19 and cancer. Expression of receptors like angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) increases COVID-19 susceptibility. SARS-CoV-2 infection might increase cancer susceptibility and accelerate cancer progression through mechanisms involving cytokine storm, tissue hypoxia, impaired T-cell responses, autophagy, neutrophil activation, and oxidative stress. These mechanisms collectively contribute to immune suppression, hindered apoptosis, and altered cellular signaling in the tumor microenvironment, creating conditions favorable for tumor growth, metastasis, and recurrence. Approved vaccines and their impact on cancer patients along-with new clinical trials are also described.
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来源期刊
CiteScore
12.30
自引率
0.00%
发文量
218
审稿时长
32 days
期刊介绍: BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
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