MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

• Published in: International journal of molecular sciences Vol. 21; no. 12; p. 4370
• Main Authors: Climent, Montserrat, Viggiani, Giacomo, Chen, Ya-Wen, Coulis, Gerald, Castaldi, Alessandra
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 19.06.2020; MDPI
• Subjects: Antioxidants; cardiac disease; Cardiomyocytes; Cardiomyopathy; Cell death; Chronic obstructive pulmonary disease; Congestive heart failure; Coronary artery disease; Crosstalk; Dehydrogenases; Deoxyribonucleic acid; Diabetes mellitus; DNA; DNA damage; Enzymes; Fibrosis; Gene expression; Gene Expression Regulation; Heart; Heart Diseases - genetics; Heart Diseases - metabolism; Homeostasis; Humans; Hypertrophy; Ischemia; Kinases; Lung cancer; Lung diseases; Lung Diseases - genetics; Lung Diseases - metabolism; MicroRNAs; MicroRNAs - genetics; miRNA; Myocardial infarction; Nitric oxide; Obstructive lung disease; Oxidative Stress; Post-transcription; Proteins; pulmonary disease; Reactive Oxygen Species - metabolism; Reperfusion; Respiration; Respiratory distress syndrome; Review; RNA polymerase; ROS; Transcription factors; microRNAs; cardiac disease; pulmonary disease; oxidative stress; ROS
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21124370

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.