PMC:7534795 / 62648-63906 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7534795","sourcedb":"PMC","sourceid":"7534795","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7534795","text":"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, 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