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1.
Int J Mol Sci ; 22(19)2021 Sep 30.
Article in English | MEDLINE | ID: covidwho-1463706

ABSTRACT

In hearts, calcium (Ca2+) signaling is a crucial regulatory mechanism of muscle contraction and electrical signals that determine heart rhythm and control cell growth. Ca2+ signals must be tightly controlled for a healthy heart, and the impairment of Ca2+ handling proteins is a key hallmark of heart disease. The discovery of microRNA (miRNAs) as a new class of gene regulators has greatly expanded our understanding of the controlling module of cardiac Ca2+ cycling. Furthermore, many studies have explored the involvement of miRNAs in heart diseases. In this review, we aim to summarize cardiac Ca2+ signaling and Ca2+-related miRNAs in pathological conditions, including cardiac hypertrophy, heart failure, myocardial infarction, and atrial fibrillation. We also discuss the therapeutic potential of Ca2+-related miRNAs as a new target for the treatment of heart diseases.


Subject(s)
Atrial Fibrillation/genetics , Calcium Signaling/genetics , Calcium/metabolism , Heart Failure/genetics , MicroRNAs/genetics , Myocardial Infarction/genetics , Animals , Atrial Fibrillation/metabolism , Atrial Fibrillation/therapy , Gene Expression Regulation , Heart Failure/metabolism , Heart Failure/therapy , Humans , Myocardial Contraction/genetics , Myocardial Infarction/metabolism , Myocardial Infarction/therapy
2.
Biomark Med ; 15(13): 1167-1175, 2021 09.
Article in English | MEDLINE | ID: covidwho-1379920

ABSTRACT

Aim: To investigate whether C-reactive protein/albumin ratio (CAR) has an association with new onset atrial fibrillation (NOAF) in SARS-CoV-2. Materials & methods: This study included 782 patients with SARS-CoV-2 infection, who were hospitalized in Turkey. The end point of the study was an occurrence of NOAF. Results: NOAF was identified in 41 patients (5.2%). Subjects who developed NOAF had a higher CAR compared with those who did not develop NOAF (p < 0.001). In the multivariate logistic regression analysis the CAR (odds ratio = 2.879; 95% CI: 1.063-7.793; p = 0.037) was an independent predictor of NOAF. Conclusion: A high level of CAR in blood samples is associated with an increased risk of developing NOAF in SARS-CoV-2.


Subject(s)
Albumins/metabolism , Atrial Fibrillation/metabolism , C-Reactive Protein/metabolism , COVID-19/complications , Aged , Atrial Fibrillation/complications , COVID-19/virology , Female , Humans , Male , Middle Aged , SARS-CoV-2/isolation & purification , Turkey
3.
Biomark Med ; 15(13): 1167-1175, 2021 09.
Article in English | MEDLINE | ID: covidwho-1362210

ABSTRACT

Aim: To investigate whether C-reactive protein/albumin ratio (CAR) has an association with new onset atrial fibrillation (NOAF) in SARS-CoV-2. Materials & methods: This study included 782 patients with SARS-CoV-2 infection, who were hospitalized in Turkey. The end point of the study was an occurrence of NOAF. Results: NOAF was identified in 41 patients (5.2%). Subjects who developed NOAF had a higher CAR compared with those who did not develop NOAF (p < 0.001). In the multivariate logistic regression analysis the CAR (odds ratio = 2.879; 95% CI: 1.063-7.793; p = 0.037) was an independent predictor of NOAF. Conclusion: A high level of CAR in blood samples is associated with an increased risk of developing NOAF in SARS-CoV-2.


Subject(s)
Albumins/metabolism , Atrial Fibrillation/metabolism , C-Reactive Protein/metabolism , COVID-19/complications , Aged , Atrial Fibrillation/complications , COVID-19/virology , Female , Humans , Male , Middle Aged , SARS-CoV-2/isolation & purification , Turkey
4.
Eur Rev Med Pharmacol Sci ; 24(23): 12609-12622, 2020 12.
Article in English | MEDLINE | ID: covidwho-995022

ABSTRACT

OBJECTIVE: In human pathology, SARS-CoV-2 utilizes multiple molecular pathways to determine structural and biochemical changes within the different organs and cell types. The clinical picture of patients with COVID-19 is characterized by a very large spectrum. The reason for this variability has not been clarified yet, causing the inability to make a prognosis on the evolution of the disease. MATERIALS AND METHODS: PubMed search was performed focusing on the role of ACE 2 receptors in allowing the viral entry into cells, the role of ACE 2 downregulation in triggering the tissue pathology or in accelerating previous disease states, the role of increased levels of Angiotensin II in determining endothelial dysfunction and the enhanced vascular permeability, the role of the dysregulation of the renin angiotensin system in COVID-19 and the role of cytokine storm. RESULTS: The pathological changes induced by SARS-CoV-2 infection in the different organs, the correlations between the single cell types targeted by the virus in the different human organs and the clinical consequences, COVID-19 chronic pathologies in liver fibrosis, cardiac fibrosis and atrial arrhythmias, glomerulosclerosis and pulmonary fibrosis, due to the systemic fibroblast activation induced by angiotensin II are discussed. CONCLUSIONS: The main pathways involved showed different pathological changes in multiple tissues and the different clinical presentations. Even if ACE2 is the main receptor of SARS-CoV-2 and the main entry point into cells for the virus, ACE2 expression does not always explain the observed marked inter-individual variability in clinical presentation and outcome, evidencing the complexity of this disorder. The proper interpretation of the growing data available might allow to better classifying COVID-19 in human pathology.


Subject(s)
Angiotensin II/metabolism , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/metabolism , Cardiomyopathies/metabolism , Cytokine Release Syndrome/metabolism , Endothelium, Vascular/physiopathology , Liver Cirrhosis/metabolism , Systemic Inflammatory Response Syndrome/metabolism , Thrombosis/metabolism , Angiotensin I/metabolism , Atrial Fibrillation/metabolism , Atrial Fibrillation/physiopathology , Blood Coagulation , COVID-19/pathology , COVID-19/physiopathology , Capillary Permeability , Cardiomyopathies/pathology , Cardiomyopathies/physiopathology , Cytokine Release Syndrome/physiopathology , Cytokines/metabolism , Fibroblasts/metabolism , Fibroblasts/pathology , Fibrosis , Humans , Liver Cirrhosis/pathology , Liver Cirrhosis/physiopathology , Myocarditis/metabolism , Myocarditis/pathology , Myocarditis/physiopathology , Receptors, Coronavirus/metabolism , Renin-Angiotensin System , SARS-CoV-2/metabolism , Systemic Inflammatory Response Syndrome/physiopathology , Thrombosis/physiopathology , Virus Internalization
5.
FASEB J ; 34(9): 11347-11354, 2020 09.
Article in English | MEDLINE | ID: covidwho-691159

ABSTRACT

A relationship between COVID-19 infection and an increasing incidence of atrial fibrillation has been observed. However, the underlying pathophysiology as a precipitant to AF has not been reviewed. This paper will consider the possible pathological and immunological AF mechanisms as a result, of COVID-19 infection. We discuss the role myocardial microvascular pericytes expressing the ACE-2 receptor and their potential for an organ-specific cardiac involvement with COVID-19. Dysfunctional microvascular support by pericytes or endothelial cells may increase the propensity for AF via increased myocardial inflammation, fibrosis, increased tissue edema, and interstitial hydrostatic pressure. All of these factors can lead to electrical perturbances at the tissue and cellular level. We also consider the contribution of Angiotensin, pulmonary hypertension, and regulatory T cells as additional contributors to AF during COVID-19 infection. Finally, reference is given to two common drugs, corticosteroids and metformin, in COVID-19 and how they might influence AF incidence.


Subject(s)
Atrial Fibrillation/etiology , Coronavirus Infections/complications , Pneumonia, Viral/complications , Angiotensin-Converting Enzyme 2 , Atrial Fibrillation/metabolism , COVID-19 , Coronavirus Infections/metabolism , Endothelial Cells/metabolism , Humans , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pericytes/metabolism , Pneumonia, Viral/metabolism , Renin-Angiotensin System
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