Using mechanism-based combinations of HS-donors to maximize the cardioprotective action of HS.

HS-donors are cardioprotective in ischemia/reperfusion (I/R) injury. Some HS-donors exert their beneficial effects in a nitric oxide (NO)-dependent manner, while others act using NO-independent pathways. The aims of the present study were to (i) evaluate whether HS-donors with distinct pharmacodynamic properties act synergistically in I/R injury and (ii) determine if HS-donors remain cardioprotective in obese mice.

Orally Bioavailable Enzymatic Inhibitor of CD38, , Protects against Ischemia/Reperfusion Injury in the Murine Heart.

CD38 is one of the major nicotinamide adenine dinucleotide (NAD)- and nicotinamide adenine dinucleotide phosphate (NADP)-consuming enzymes in mammals. NAD, NADP, and their reduced counterparts are essential coenzymes for numerous enzymatic reactions, including the maintenance of cellular and mitochondrial redox balance. CD38 expression is upregulated in age-associated inflammation as well as numerous metabolic diseases, resulting in cellular and mitochondrial dysfunction.