Kell Douglas B, Khan Muhammed Asad, Kane Binita, Lip Gregory Y H, Pretorius Etheresia
Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK.
The Novo Nordisk Foundation Centre for Biosustainability, Building 220, Chemitorvet 200, Technical University of Denmark, 2800 Kongens Lyngby, Denmark.
J Pers Med. 2024 Jan 31;14(2):170. doi: 10.3390/jpm14020170.
Postural orthostatic tachycardia syndrome (POTS) is a common accompaniment of a variety of chronic, inflammatory diseases, including long COVID, as are small, insoluble, 'fibrinaloid' microclots. We here develop the argument, with accompanying evidence, that fibrinaloid microclots, through their ability to block the flow of blood through microcapillaries and thus cause tissue hypoxia, are not simply correlated with but in fact, by preceding it, may be a chief intermediary cause of POTS, in which tachycardia is simply the body's exaggerated 'physiological' response to hypoxia. Similar reasoning accounts for the symptoms bundled under the term 'fatigue'. Amyloids are known to be membrane disruptors, and when their targets are nerve membranes, this can explain neurotoxicity and hence the autonomic nervous system dysfunction that contributes to POTS. Taken together as a system view, we indicate that fibrinaloid microclots can serve to link POTS and fatigue in long COVID in a manner that is at once both mechanistic and explanatory. This has clear implications for the treatment of such diseases.
体位性直立性心动过速综合征(POTS)是多种慢性炎症性疾病(包括长新冠)的常见伴随症状,小的、不溶性的“纤维样”微血栓也是如此。我们在此提出观点并附上证据,即纤维样微血栓通过其阻断微毛细血管内血流从而导致组织缺氧的能力,不仅与POTS相关,实际上,在其之前,可能是POTS的主要中间原因,其中心动过速仅仅是身体对缺氧的过度“生理”反应。类似的推理可以解释“疲劳”这一术语所涵盖的症状。已知淀粉样蛋白是膜破坏剂,当其作用靶点是神经膜时,这可以解释神经毒性,进而解释导致POTS的自主神经系统功能障碍。从系统角度综合来看,我们指出纤维样微血栓可以以一种兼具机制性和解释性的方式,将长新冠中的POTS和疲劳联系起来。这对这类疾病的治疗具有明确的意义。