Abstract
With respect to structural and functional cardiac disorders, heart failure (HF) is divided into HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Oxidative stress contributes to the development of both HFrEF and HFpEF. Identification of a broad spectrum of reactive oxygen species (ROS)-induced pathways in preclinical models has provided new insights about the importance of ROS in HFrEF and HFpEF development. While current treatment strategies mostly concern neuroendocrine inhibition, recent data on ROS-induced metabolic pathways in cardiomyocytes may offer additional treatment strategies and targets for both of the HF forms. The purpose of this article is to summarize the results achieved in the fields of: (1) ROS importance in HFrEF and HFpEF pathophysiology, and (2) treatments for inhibiting ROS-induced pathways in HFrEF and HFpEF patients. ROS-producing pathways in cardiomyocytes, ROS-activated pathways in different HF forms, and treatment options to inhibit their action are also discussed.
Highlights
With respect to structural and functional cardiac disorders, chronic heart failure (CHF)is classified into heart failure (HF) with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF)
Mitochondrial damage, including enzymes involved in metabolic pathways, outer mitochondrial membrane (OMM) and inner mitochondrial membrane (IMM) proteins, electron transport chain (ETC) protein acetylation and Ca2+ channels were found to be more related to reactive oxygen species (ROS)-induced cardiomyocyte damage and CHF progression in HF with reduced ejection fraction (HFrEF) patients
Some groups of compounds were investigated for their effect in oxidative stress-induced myocardial damage/remodeling reduction in CHF development including: (1) adenosine monophosphateactivated protein kinase (AMPK) activators, (2) renin-angiotensin system inhibitors
Summary
With respect to structural and functional cardiac disorders, chronic heart failure (CHF). The agents referred to are produced in the cells by the mitochondria and enzymes, such as lipoxygenases and cyclooxygenases, under normal conditions [13] Some processes, such as apoptosis, immune system reactions, differentiation, activation of several transcriptional factors, cellular signaling pathways and induction of a mitogenic response require the presence of some ROS [14]. O2− takes part in signal transmission by: (1) causing post-translation redox modifications of proteins [15], (2) hydroxylation (addition of an HO group) [16], and (3) S-nitrosylation (oxidation of cysteine by NO) [17] By these means, the reactivity, stability and conformation of the affected molecules is altered [17]. ROS damage mitochondrial phospholipid membranes and, as a consequence, induce mitochondrial oxidative stress, leading to molecular mechanisms that contribute to the development and progression of heart failure [25]
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