Gallic acid (GA) is a bioactive phytoconstituent that has been reported to prevent a number of diseases. However, there is no systematic review to-date on its anti-diabetic and cardioprotective potential including molecular mechanisms for such activities. This review aims to summarize the anti-diabetic and cardioprotective effects of GA and further propose a molecular mechanism of its anti-diabetic effects. Accumulation of associated literature was conducted through the use of databases including Google Scholar, PubMed, Web of Science, Science Direct and Scopus databases. Articles published until December 2018 were extracted and all the retracted articles were sorted based on the inclusion and exclusion criteria and relevant articles were further consulted for necessary information. We have found substantial investigations in animals and cultured cells that supports anti-diabetic and cardioprotective effects of GA with several underlying mechanisms including antioxidant enzyme systems and non-enzymatic defense mechanisms. The reported antioxidant activity of GA as well as the modulation of some key proteins linked to diabetes could be a part of the mechanisms by which GA showed anti-diabetic effect. In summary, it is evident that GA is one of the promising dietary phytochemicals that could be beneficial for the treatment and management of diabetes and associated myocardial damage. Abbreviation: AGEs: advanced glycation end products; Akt: protein kinase B; ALT: alanine transaminase; AMPKα: AMP-activated protein kinase-alpha; AMPKγ: AMP-activated protein kinase-gamma; ANP: atrial natriuretic peptide; AST: aspartate transaminase; b.w: body weight; CAT: catalase; CK: creatine kinase; CK-MB: creatine kinase-myoglobin binding; CPK: creatine phosphokinase; CRP: C-reactive protein; CsA: cyclosporine A; CVDs: cardiovascular diseases; Cx43: gap junction protein Connexin 43; CYP: cyclophosphamide; CTGF: connective tissue growth factor; DM: diabetes mellitus; D-MI: diabetes with myocardial infraction; DOX: doxorubicin; ECM: extracellular matrix; ERKs: extracellular signal-regulated kinases; GA: gallic acid; GSIS: glucose-stimulated insulin secretion; GLUT4: glucose transporter protein 4; GLUT2: glucose transporter protein 2; GR: glutathione reductase; GSH: reduced Glutathione reductase; GST: glutathione-S-transferase; GATA4: transcription factor GATA-4; HDL: high-density lipoprotein; H9c2(2-1): embryonic rat cardiomyocyte cell line; iNOS: inducible nitric oxide synthase; ISO: isoproterenol; JNKs: c-Jun N-terminal kinases; L-NAME: N-nitro-L-arginine methyl ester; LDL-C: LDL-cholesterol; LDH: lactate dehydrogenase; LDL: low-density lipoprotein; LOOH: lipid hydroperoxides; LPO: lipid peroxidation; LV: left ventricular; MDA: malondialdehyde; MHC-β: myosin heavy chain beta; MI: myocardial infraction; MMP: matrix metalloproteinase; Na⁺/K⁺-ATPase: sodium-potassium adenosine triphosphatase; Nox2: NADPH oxidase 2; PCO: protein carbonyls; PGC1α: peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PI: plasma insulin; PI3K: phosphatidylinositol 3-kinase; PPARγ: peroxisome proliferator-activated receptors- gamma; RAGE: receptor for AGE; ROS: reactive oxygen species; SC: serum creatinine; SOD: superoxide dismutase; GPx: glutathione peroxidase; SHRs: spontaneously hypertensive rats; STZ: Steptozotocin; TBARS: thiobarbituric acid reactive substances; TC: total cholesterol; TG: triglyceride; TGF-β: transforming growth factor beta; TIMP: tissue inhibitor of metalloproteinases; TNF-α: tumor necrosis factor-alpha; TnI: troponin-I; TZDs: thiazolidinediones; UA: uric acid; UCP2: uncoupling protein 2; XO: xanthine oxidase.