Skip to main content
. 2013 May 12;2013:191823. doi: 10.1155/2013/191823

Table 1.

PUFAs and cardiovascular disease.

PUFA effects
(1) Anti-inflammatory   (a) ↓NF-κB activation
  (b) EPA and DHA compete with AA for COX & 5-lipo-oxygenase enzymatic sites
            ⇓
 Reduce the production of IL-1, IL-6, and TNF-α
   (c) ↑Anti inflammatory eicosanoids

(2) Cardiac energetic    (a) ↑ATP generation
   (b) ↓O2 consumption
   (c) ↓Sarcoplasmic reticulum calcium concentration
            ⇓
 Maintain normal mitochondrial function

(3) Antiarrhythmic    (a) ↑Ca2+/Mg2+ ATPase activity
   (b) Inhibit fast voltage-dependent Na+ channels (I Na)
   (c) Inhibit L-type Ca2+ channels (I Ca,L)
            ⇓
 Membrane stabilization
   (d) Reduced automaticity
   (e) Increased relative refractory period

(4) Hemodynamics    (a) Improved endothelium-independent and dependent vasodilatation
   (b) ↓ET-1
   (c) ↑NO
            ⇓
 Improved endothelium dysfunction

(5) Ventricular remodeling and fibrosis    (a) ↑PPARγ → ↑adiponectin
            ⇓
 Attenuates ventricular remodeling

(6) Vascular    (a) ↓Platelet aggregation via ↓TXA2
   (b) ↓VCAM-1, ELAM-1, ICAM-1
   (c) ↓monocyte endothelial adherence via ↓PAF

EPA: eicosapentaenoic acid; DHA: docosahexaenoic acid; AA: arachidonic acid; ET-1: endothelin-1; NO: nitric oxide; PPAR-γ: peroxisome proliferation-activated receptors-γ; TX A2: thromboxane A2; VCAM-1: vascular cell adhesion protein 1; ELAM-1: endothelial leukocyte adhesion molecule-1; ICAM-1: intercellular adhesion molecule-1; PAF: platelet activating factor; COX: cyclooxygenase.