The Role of MicroRNAs in Dilated Cardiomyopathy: New Insights for an Old Entity.
Elena Alonso-VillaFernando BonetFrancisco Hernandez-TorresÒscar CampuzanoGeorgia Sarquella BrugadaMaribel Quezada-FeijoóMónica RamosAlipio MangasRocío ToroPublished in: International journal of molecular sciences (2022)
Dilated cardiomyopathy (DCM) is a clinical diagnosis characterized by left ventricular or biventricular dilation and systolic dysfunction. In most cases, DCM is progressive, leading to heart failure (HF) and death. This cardiomyopathy has been considered a common and final phenotype of several entities. DCM occurs when cellular pathways fail to maintain the pumping function. The etiology of this disease encompasses several factors, such as ischemia, infection, autoimmunity, drugs or genetic susceptibility. Although the prognosis has improved in the last few years due to red flag clinical follow-up, early familial diagnosis and ongoing optimization of treatment, due to its heterogeneity, there are no targeted therapies available for DCM based on each etiology. Therefore, a better understanding of the mechanisms underlying the pathophysiology of DCM will provide novel therapeutic strategies against this cardiac disease and their different triggers. MicroRNAs (miRNAs) are a group of small noncoding RNAs that play key roles in post-transcriptional gene silencing by targeting mRNAs for translational repression or, to a lesser extent, degradation. A growing number of studies have demonstrated critical functions of miRNAs in cardiovascular diseases (CVDs), including DCM, by regulating mechanisms that contribute to the progression of the disease. Herein, we summarize the role of miRNAs in inflammation, endoplasmic reticulum (ER) stress, oxidative stress, mitochondrial dysfunction, autophagy, cardiomyocyte apoptosis and fibrosis, exclusively in the context of DCM.
Keyphrases
- oxidative stress
- heart failure
- left ventricular
- endoplasmic reticulum
- cardiac resynchronization therapy
- endoplasmic reticulum stress
- cell death
- cardiovascular disease
- blood pressure
- acute myocardial infarction
- metabolic syndrome
- angiotensin ii
- induced apoptosis
- ischemia reperfusion injury
- multiple sclerosis
- transcription factor
- gene expression
- dna damage
- mitral valve
- acute heart failure
- single cell
- signaling pathway
- early onset
- endothelial cells
- heat shock
- copy number
- cell cycle arrest
- aortic valve