Table 1.

List of preclinical and clinical studies indicating SPMs and eicosanoids roles in cardiovascular medicine.

SPMs action in preclinical studies of ischemic heart disease
Year	Specific SPMs in Disease Pathology	Mechanism of Action of SPMs	Refs.
2017, 2018	LXA4/ AT-LXA4 (Myocardial Infarction)	↑ activation of FPR2 receptor ↓ left ventricular remodeling ↑ mobilization of cytosolic calcium ↓ activation of the calcium-sensitive kinase ↑ calcium/calmodulin-dependent protein kinase II	13,14
2015, 2017, 2020	RvD1 (Myocardial Infarction and Muscle Injury)	↑ activation FPR2 receptor ↓ neutrophil swarming ↑ macrophage clearance ↓ muscle inflammatory cytokines ↓ pro-inflammatory macrophage infiltration ↓ LV remote hypertrophy	12,39,58
2019, 2020	Maresins (Myocardial Infarction)	↑ macrophage phagocytosis and efferocytosis ↓ infarct size and inflammatory mediators	32,56
2014	18 HEPE (Pressure overload-induced inflammation and fibrosis)	↑ generation of cardiac fibroblasts ↑ macrophages clearance	59

SPMs roles in Human Studies
Year	Disease Pathology	Mechanism of Action of SPMs	Refs.
2019	Acute Myocardial Infarction	↑ physiological initial inflammation and ↑ SPMs activation prior to troponin during the onset of MI confirmed by ST elevation	49
2020	Acute Myocardial Infarction	↑ RvE1 in white patients than black patients after MI ↑ activation of resolution and inflammation after MI and marked by SPMs biosynthesis	50
2019, 2020	Peripheral Artery Disease	↑ pro‐resolution phenotype of leukocytes ↑ resolving effects through biosynthesis of SPMs	60
2020	Hypertension/Borderline CVD	↑ eicosanoids derived from arachidonic acids are pro-inflammatory (12 HHTrE, TXA2, TXB2 etc.) ↑ ω‐3 metabolites are crucial for the regulation of blood pressure and inflammation	61

Abbreviations: RvD1; Resolvin D1, LXA4/ AT-LXA4; lipoxin A₄ and aspirin-tirggered lipoxin A₄, FPR2; Formyl-peptide receptor-2, 18 HEPE; 18-hydroxyeicosapentaenoic acid, TXA₂; Thromboxane A2, TXB2; Thromboxane B2.