Based on several clinical reports, COVID-19 patients with severe ALI/ARDS may also suffer from increased risk of sepsis and cardiac arrest (Huang et al., 2020). Accumulating reports have indicated that n-3 PUFAs could improve resolution of inflammation, sepsis survival and precondition the heart against septic cardiomyopathy (Korner et al., 2018; Leger et al., 2019). In this review, we propose that n-3 PUFAs can protect against and ameliorate cardiovascular complications associated with COVID-19 mainly due to their immunomodulatory features, antioxidant potential as well as their ability to maintain tissue homeostasis. This section will highlight the cardioprotective mechanisms of n-3 PUFAs and their metabolites hypothesizing how n-3 PUFAs might have a supportive adjuvant utility in treating and protecting against cardiac complications associated with COVID-19 (Fig. 2 ).
Fig. 2 Potential cardioprotective mechanisms of n-3 PUFAs in the setting of COVID-19. (A) N-3 PUFAs ameliorate uncontrolled immune responses and exert anti-inflammatory effects via several mechanisms. (B) N-3 PUFAs attenuate the vicious cycle/interaction of mitochondrial dysfunction and aggravated immune response. (C) N-3 PUFAs have the capability to attenuate viral infections via both direct effects on membrane integrity and indirect mechanisms through activating the humoral response to decrease overall viral load. (D) N-3 PUFAs have the ability to regulate the RAAS system in the favor of the vasodilatory, the anti-inflammatory and the cardioprotective ACE2/Ang (1–7) effectors. (E) N-3 PUFAs enhance antioxidant capacity and attenuate oxidative stress in the tissue. (F) N-3 PUFAs ameliorate coagulopathy by exerting anti-thrombotic effects. (G) The triglyceride-lowering effect of n-3 PUFAs may play a key role in blunting the exaggerated inflammation observed in patients with COVID-19. ACE, Angiotensin-converting enzyme; Ang, Angiotensin; CRP, C-reactive protein; IL, Interleukin; mtDNA, Mitochondrial DNA; PUFA, Poly unsaturated fatty acid; ROS, Reactive oxygen species; TGs, Triglycerides; TNF-α, Tumor necrosis factor alpha; TX, Thromboxane.