Abstract
Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.
Highlights
Pathologies of the cardiac and pulmonary systems in their broad spectrum of etiology, including among others heart failure, cardiomyopathies, lung cancer, and acute lung injury, rank among the leading causes of mortality and have a significant impact on health and healthcare of patients
The authors did not investigate the specific gene targeting through which miR-126 exerts its antioxidant function, they showed a direct activation of PI3K/Akt/SK-3b and ERK1/2 signaling pathway by miR-126, which contributed to the biological functions of endothelial progenitor cells (EPC) [70]
The present review extensively summarizes the importance of the crosstalk between miRNAs and reactive oxygen species (ROS) in cardiac and pulmonary diseases
Summary
Pathologies of the cardiac and pulmonary systems in their broad spectrum of etiology, including among others heart failure, cardiomyopathies, lung cancer, and acute lung injury, rank among the leading causes of mortality and have a significant impact on health and healthcare of patients. Over the past few years, numerous studies have reported concomitant expression signature of reactive oxygen species (ROS) and small noncoding microRNAs (miRNAs), which are key players in many pathophysiological processes [1,2] This recent focus set the premise to study the crosstalk between redox signaling and disease-specific miRNAs in the cardiac and pulmonary systems. In line with this, targeting of ARSB by miR-154-5p led to increased ROS production and activation of the NF-κB signaling pathway, contributing, at least in part, to cardiac hypertrophy [39]. In contrast with the studies described above, in which oxidative stress was induced by overexpression of miRNAs, a similar effect was achieved by the downregulation of miR-448-3p, leading to cardiac dysfunction. The authors reported that miR-448-3p downregulation promotes cellular oxidative stress and intracellular calcium (Ca2+) signaling in cardiac hypertrophy [45]
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