A potential role for Galectin-3 inhibitors in the treatment of COVID-19

A potential role for Galectin-3 inhibitors in the treatment of COVID-19
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DOI:
10.7717/peerj.9392
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发表时间:
2020-06-15
期刊:
影响因子:
2.7
通讯作者:
Velpula, Kiran K.
Velpula, Kiran K.
中科院分区:
生物学3区
文献类型:
--
作者:
Caniglia, John L.;Guda, Maheedhara R.;Velpula, Kiran K.

文献摘要

被引文献

相似文献

2019冠状病毒病(COVID-19)的病原体严重急性呼吸系统综合征冠状病毒2(SARS-CoV 2)的爆发已被世界卫生组织宣布为全球大流行。由于没有治疗COVID-19的标准护理,迫切需要确定可能有效的治疗方法。最近的证据表明,细胞因子释放综合征的发展是COVID-19患者死亡的主要原因,在患者中观察到白细胞介素-6(IL-6)和肿瘤坏死因子α(TNF-α)水平升高。半乳糖凝集素-3(Galectin-3,Gal-3)是一种动物凝集素,与多种炎症性疾病的发病过程有关。小分子Gal-3的抑制剂已经显示在体外降低IL-6和TNF-α的水平,并且已经显示出体内抗炎作用。此外,包括SARS-CoV 2的β-冠状病毒科的刺突蛋白中的关键结构域在形态上与人Gal-3几乎相同。这些刺突蛋白对于病毒进入宿主细胞至关重要。在此,我们对现有文献进行了系统综述,并推动了对Gal-3抑制剂治疗COVID-19的进一步研究。此外,我们提出了一种双重机制,通过这种机制,Gal-3抑制可能有益于COVID-19的治疗,既抑制宿主炎症反应,又阻止病毒附着于宿主细胞。
The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), the causative agent of coronavirus disease 2019 (COVID-19), has been declared a global pandemic by the World Health Organization. With no standard of care for the treatment of COVID-19, there is an urgent need to identify therapies that may be effective in treatment. Recent evidence has implicated the development of cytokine release syndrome as the major cause of fatality in COVID-19 patients, with elevated levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) observed in patients. Galectin-3 (Gal-3) is an animal lectin that has been implicated in the disease process of a variety of inflammatory conditions. Inhibitors of the small molecule Gal-3 have been shown to reduce the levels of both IL-6 and TNF-alpha in vitro and have shown anti-inflammatory effects in vivo. Additionally, a key domain in the spike protein of beta-coronaviridae, a genus which includes SARS-CoV2, is nearly identical in morphology to human Gal-3. These spike proteins are critical for the virus' entry into host cells. Here we provide a systematic review of the available literature and an impetus for further research on the use of Gal-3 inhibitors in the treatment of COVID-19. Further, we propose a dual mechanism by which Gal-3 inhibition may be beneficial in the treatment of COVID-19, both suppressing the host inflammatory response and impeding viral attachment to host cells.