Review Article

Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions—A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology

Table 1

Properties of the main antioxidant therapeutics.

Components of standard heart failure therapy that possess antioxidant properties
ACEi, ARBs, ARNi, antialdosterone drugs: interference with RAAS signaling
Carvedilol: 1- and 2-adrenergic receptor blocker that also increase NO production or decrease inactivation
3AR agonists: enhancement of myocardial 3-adrenergic coupling with NO-cGMP signaling
ARNi: enhancement of NPs/cGMP/PKG pathway

Drugs with redox effect that are not mainstream therapeutic approach in heart failure
PDE5 inhibition and BH4 supplementation: potentiating NO/cGMP/PKG signaling
Statins: NADPH oxidase inhibitors
Allopurinol: xanthine oxidases inhibitor
Ranolazine: inhibitor of elevated late
MAO inhibitors: blunting ROS production from MAOs

Novel therapeutic compounds that target ROS/RNS signaling pathways
SS-31 (MTP-131, Bendavia): direct action on mitochondrial function
Resveratrol: preservation of the LKB1-AMPK-eNOS signaling axis
HNO donors: improving Ca2+ cycling and myofilament Ca2+ sensitivity

ARNi: angiotensin receptor-neprilysin inhibitor.
AMPK: AMP-activated protein kinase.
NPs: natriuretic peptides.