Myocardial fibrosis impairs cardiac function, in addition to facilitating arrhythmias and ischemia, and thus influences the evolution and outcome of cardiac diseases. Its assessment is therefore clinically relevant. Although tissue biopsy is the gold standard for the diagnosis of myocardial fibrosis, a number of circulating biomarkers have been proposed for the noninvasive assessment of this lesion. A review of the published clinical data available on these biomarkers shows that most of them lack proof that they actually reflect the myocardial accumulation of fibrous tissue. In this "call to action" article, we propose that this absence of proof may lead to misinterpretations when considering the incremental value provided by the biomarkers with respect to traditional diagnostic tools in the clinical handling of patients. We thus argue that strategies are needed to more strictly validate whether a given circulating biomarker actually reflects histologically proven myocardial fibrosis before it is applied clinically.
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http://dx.doi.org/10.1016/j.jacc.2015.04.026 | DOI Listing |
Circ Res
December 2024
Cardiovascular Research Center, Cardiology Division (E.A.-B., S.J.R., B.F.M., D.E.S.).
J Inflamm Res
December 2024
Department of Cardiothoracic Surgery, Changzheng Hospital, Naval Medical University, Shanghai, People's Republic of China.
Background: Cardiac macrophages are a heterogeneous population with high plasticity and adaptability, and their mechanisms in heart failure (HF) remain poorly elucidated.
Methods: We used single-cell and bulk RNA sequencing data to reveal the heterogeneity of non-cardiomyocytes and assess the immunoreactivity of each subpopulation. Additionally, we employed four integrated machine learning algorithms to identify macrophage-related genes with diagnostic value, and in vivo validation was performed.
Heliyon
December 2024
Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Heart failure (HF) syndrome is of great interest as an emerging epidemic. Due to the increasing elderly population worldwide, the total number of HF patients is increasing every day. This disease places a significant economic burden on the healthcare and treatment systems of developing societies, and this situation is very concerning.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
December 2024
Department of Medicine, Division of Cardiology, University of Colorado Anschutz Medical Campus; Aurora, CO, USA.
Bromodomain and extra-terminal domain (BET) proteins, including BRD4, bind acetylated chromatin and co-activate gene transcription. A BET inhibitor, JQ1, prevents and reverses pathological cardiac remodeling in preclinical models of heart failure. However, the underlying cellular mechanisms by which JQ1 improves cardiac structure and function remain poorly defined.
View Article and Find Full Text PDFBackground: Loss of stromal interaction molecule 1 (STIM1) expression in smooth muscle cells protects against ischemia-reperfusion (I/R) injury. Whether and how decreased STIM1 expression in cardiomyocytes (CM) impacts cardiac remodeling in response to I/R injury remains unknown.
Objective: To examine mechanisms by which decreased CM-STIM1 expression in the adult heart modulates cardiac function before and after I/R injury.
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