Roberto Motterlini

TL;DR: An overview of the physiology of CO is provided, the effects of CO gas and CO-releasing molecules in preclinical animal models of cardiovascular disease, inflammatory disorders and organ transplantation are summarized, and the development and therapeutic options for the exploitation of this simple gaseous molecule are discussed.

TL;DR: It is demonstrated that induction of HO-1 by curcumin and CAPE requires the activation of the Nrf2/ARE pathway, and using antibodies and specific inhibitors of the mitogen-activated protein kinase (MAPK) pathways, data is provided implicating p38 MAPK inCurcumin-mediated ho-1 induction.

TL;DR: It is reported that a series of transition metal carbonyls, termed here carbon monoxide-releasing molecules (CO-RMs), liberate CO to elicit direct biological activities and caused sustained vasodilation in precontracted rat aortic rings, attenuated coronary vasoconstriction in hearts ex vivo, and significantly reduced acute hypertension in vivo.

TL;DR: Data indicate that curcumin is a potent inducer of HO-1 in vascular endothelial cells and that increased heme oxygenase activity is an important component inCurcumin-mediated cytoprotection against oxidative stress.

TL;DR: It is found that tricarbonylchloro(glycinato)ruthenium(II) (CORM‐3) is stable in water at acidic pH but in physiological buffers rapidly liberates CO in solution, corroborate the notion that transition metal carbonyls could be used as carriers to deliver CO and highlight the bioactivity and potential therapeutic features of CO‐RMs in the mitigation of cardiac dysfunction.