Role of Selected miRNAs as Diagnostic and Prognostic Biomarkers in Cardiovascular Diseases, Including Coronary Artery Disease, Myocardial Infarction and Atherosclerosis

Mir, Rashid; Elfaki, Imadeldin; Khullar, Naina; Waza, Ajaz Ahmad; Jha, Chandan Kumar; Mir, Mohammad Muzaffar; Nisa, Shamsu; Mohammad, Babar; Mir, Tahir Ahmad; Maqbool, Mohsin; Barnawi, Jameel; Albalawi, Salem Owaid; Abuduhier, Faisel M.

doi:10.3390/jcdd8020022

Cited by 33 publications

(24 citation statements)

References 118 publications

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“…Importantly, abundant and stable miRNAs can be detected in plasma, and their expression is frequently dysregulated in diseases [ 10 ]. Multiple circulation miRNAs have been reported as an ideal cluster of blood-based biomarkers for many diseases such as cancer and cardiac diseases [ 11 , 12 ]. However, the mechanisms underlying the miRNA interaction with the inflammation in HF have not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-181b Serves as a Circulating Biomarker and Regulates Inflammation in Heart Failure

et al. 2021

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Heart failure (HF) is the typical terminal stage of cardiac diseases involving inflammatory states. The function of microRNAs (miRNAs) in the progress of HF remains poorly understood. In this study, real-time PCR results showed a decreased expression of miRNA-181b (miR-181b) in HF patients compared with healthy individuals. Besides, miR-181b expressions were negatively correlated with hypersensitive C-reactive protein (hsCRP) levels in the serum of HF patients. Receiver operator characteristic (ROC) curve analysis showed that miR-181b was a diagnostic predictor of HF, and the area under the curve was 0.970 (DCM-induced HF group) and 0.962 (ICM-induced HF group). Strikingly, in HF rats induced by isoproterenol (ISO), the expression of miR-181b of heart tissue was suppressed before tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) increase, as revealed by western blot and real-time PCR. Besides, the overexpression of miR-181b also decreased the expression of TNF-α, IL-1β, and IL-6 in lipopolysaccharide- (LPS-) induced neonatal cardiomyocytes. In conclusion, our results revealed that miR-181b might be a potential biomarker for HF and provided a novel target for anti-inflammatory therapy.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-181b Serves as a Circulating Biomarker and Regulates Inflammation in Heart Failure

et al. 2021

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“…Thus, hsa-miR-933, RELB, and CCL21 may be correlated with HF and neurological disorders. Previous studies have found that miRNAs in circulating blood alone also have the potential to predict dementia and HF [38][39][40]. This is because the information in circulating blood miRNAs is suggestive of essential organismal conditions such as ischemic, cardiomyopathy, diabetes, and valvular [41][42][43][44].…”

Section: Discussionmentioning

confidence: 99%

Crosstalk between Heart Failure and Cognitive Impairment via hsa-miR-933/RELB/CCL21 Pathway

Feng

Yang

Song³

et al. 2021

BioMed Research International

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Background. The association between heart failure (HF) and cognitive impairment has received increasing attention from scholars and researchers in recent years. However, no systematic studies have been carried out yet focused on the crosstalk between heart failure and cognitive impairment via miRNAs. Methods. GSE104150, GSE53473, GSE120584, and GSE116250 with RNA-seq data and clinical data were downloaded from the GSE database. All data were statistically analysed using R software to detect DE-miRNAs and DE-mRNAs associated with both HF and cognitive impairment. Protein-protein interaction (PPI) networks were mapped, and a logistic regression model for cognitive impairment prediction was developed. Furthermore, the TTRUST database and miRWalk were used to map miRNA-transcription factor (TF) and messenger RNA (mRNA) regulatory pathways. Finally, core TFs were enriched for analysis. Results. Differentially enriched DE-miRNAs and DE-mRNAs both present in HF and cognitive impairment were determined. A logistic regression model established based on DE-miRNAs was validated to have a strong performance in cognitive impairment prediction. The core miRNA-TF-mRNA pathway was formed by mapping the PPI networks associated with the two diseases. Further GSEA was performed with V-rel reticuloendotheliosis viral oncogene homolog B (RELB) as the core TF, and the retinol metabolism and gap junction pathways were analysed. Conclusions. This study was the first attempt to predict the crosstalk and examine underlying mechanisms between HF and cognitive impairment applying bioinformatics. The findings suggested a potential hsa-miR-933/RELB/CCL21 regulatory axis correlated with HF and neurological disorders (or cognitive impairment), according to PPI networks.

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“…Cardiovascular disease is the leading cause of death in the world, including cardiac failure, coronary heart disease, myocardial infarction and atherosclerosis ( Mir et al, 2021 ). Atherosclerosis is one of the most common causes of cardiovascular disease ( Poznyak et al, 2021 ).…”

Section: Phytochemical-mediated Mitophagy In Metabolic Disordersmentioning

confidence: 99%

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

Guo

Huang

et al. 2021

Front. Cell Dev. Biol.

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Metabolic disorders include metabolic syndrome, obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease and cardiovascular diseases. Due to unhealthy lifestyles such as high-calorie diet, sedentary and physical inactivity, the prevalence of metabolic disorders poses a huge challenge to global human health, which is the leading cause of global human death. Mitochondrion is the major site of adenosine triphosphate synthesis, fatty acid β−oxidation and ROS production. Accumulating evidence suggests that mitochondrial dysfunction-related oxidative stress and inflammation is involved in the development of metabolic disorders. Mitophagy, a catabolic process, selectively degrades damaged or superfluous mitochondria to reverse mitochondrial dysfunction and preserve mitochondrial function. It is considered to be one of the major mechanisms responsible for mitochondrial quality control. Growing evidence shows that mitophagy can prevent and treat metabolic disorders through suppressing mitochondrial dysfunction-induced oxidative stress and inflammation. In the past decade, in order to expand the range of pharmaceutical options, more and more phytochemicals have been proven to have therapeutic effects on metabolic disorders. Many of these phytochemicals have been proved to activate mitophagy to ameliorate metabolic disorders. Given the ongoing epidemic of metabolic disorders, it is of great significance to explore the contribution and underlying mechanisms of mitophagy in metabolic disorders, and to understand the effects and molecular mechanisms of phytochemicals on the treatment of metabolic disorders. Here, we investigate the mechanism of mitochondrial dysfunction in metabolic disorders and discuss the potential of targeting mitophagy with phytochemicals for the treatment of metabolic disorders, with a view to providing a direction for finding phytochemicals that target mitophagy to prevent or treat metabolic disorders.

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Role of Selected miRNAs as Diagnostic and Prognostic Biomarkers in Cardiovascular Diseases, Including Coronary Artery Disease, Myocardial Infarction and Atherosclerosis

Cited by 33 publications

References 118 publications

MicroRNA-181b Serves as a Circulating Biomarker and Regulates Inflammation in Heart Failure

MicroRNA-181b Serves as a Circulating Biomarker and Regulates Inflammation in Heart Failure

Crosstalk between Heart Failure and Cognitive Impairment via hsa-miR-933/RELB/CCL21 Pathway

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

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