Coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has currently led to a global pandemic with millions of confirmed and increasing cases around the world. The novel SARS-CoV-2 not only affects the lungs causing severe acute respiratory dysfunction but also leads to significant dysfunction in multiple organs and physiological systems including the cardiovascular system. A plethora of studies have shown the viral infection triggers an exaggerated immune response, hypercoagulation and oxidative stress, which contribute significantly to poor cardiovascular outcomes observed in COVID-19 patients. To date, there are no approved vaccines or therapies for COVID-19. Accordingly, cardiovascular protective and supportive therapies are urgent and necessary to the overall prognosis of COVID-19 patients. Accumulating literature has demonstrated the beneficial effects of n-3 polyunsaturated fatty acids (n-3 PUFA) toward the cardiovascular system, which include ameliorating uncontrolled inflammatory reactions, reduced oxidative stress and mitigating coagulopathy. Moreover, it has been demonstrated the n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are precursors to a group of potent bioactive lipid mediators, generated endogenously, which mediate many of the beneficial effects attributed to their parent compounds. Considering the favorable safety profile for n-3 PUFAs and their metabolites, it is reasonable to consider n-3 PUFAs as potential adjuvant therapies for the clinical management of COVID-19 patients. In this article, we provide an overview of the pathogenesis of cardiovascular complications secondary to COVID-19 and focus on the mechanisms that may contribute to the likely benefits of n-3 PUFAs and their metabolites.
【저자키워드】 COVID-19, Inflammation, COVID-19, Coronavirus disease 2019, SARS-CoV-2, Severe acute respiratory syndrome coronavirus 2, Cardiovascular disorders, SARS-CoV, severe acute respiratory syndrome coronavirus, IFN, interferon, ARDS, acute respiratory distress syndrome, IL, interleukin, ACE, Angiotensin converting enzyme, ICU, Intensive care unit, CRP, C-reactive protein, TLR, Toll-like receptor, RNA, Ribonucleic acid, NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells, ROS, reactive oxygen species, bioactive metabolites, AA, arachidonic acid, EPA, eicosapentaenoic acid, LA, linoleic acid, LOX, lipoxygenase, PG, prostaglandin, Ang, angiotensin, ALI, Acute Lung Injury, TNF-α, tumor necrosis factor-α, LPS, lipopolysaccharide, CVD, cardiovascular disease, HF, heart failure, MI, myocardial infarction, PPAR, Peroxisome proliferator-activated receptor, COX, cyclooxygenase, n-3 polyunsaturated fatty acids, ALA, α-Linolenic acid, ARB, Angiotensin II receptor blocker, CYP, Cytochrome P450, DHA, Docosahexaenoic acid, EDP, Epoxydocosapentaenoic acid, EEQ, Epoxyeicosatetraenoic acid, GPR, G-protein coupled receptor, HDHA, Hydroxydocosahexaenoic acid, HDL-c, High density lipoprotein cholesterol, LT, Leukotriene, MERS-CoV, Middle East respiratory syndrome-related coronavirus, nCoVs, Novel coronaviruses, NLRP3, NOD, LRR and pyrin domains-containing protein 3, PMN, Polymorphonuclear neutrophils, PUFA, Polyunsaturated fatty acid, RAAS, Renin-angiotensin aldosterone system, SPM, Specialized pro-resolving mediators, TX, Thromboxane.,