Decreased Expression of Thrombospondin-1 in Failing Hearts May Favor Ventricular Remodeling

Batlle, Montserrat; Pérez‐Villa, Félix; Lázaro, A. M.; García-Pras, Ester; Vallejos, I.; Sionís, Alessandro; Castel, María Ángeles; Roig, Eulàlia

doi:10.1016/j.transproceed.2009.06.009

Cited by 21 publications

(18 citation statements)

References 10 publications

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“…TSP1 may prevent infarct expansion and cardiac dilation by limiting the influx of inflammatory cells [30] and TNC and periostin by improving the assembly and maturation of collagen fibers [12,31]. Confirming the hypothesis, myocardial biopsies from patients with end-stage heart failure show low levels of TSP1 expression [32]. However, at the same time, maintained production of matricellular proteins has the potential to cause cardiac dysfunction.…”

Section: Discusionmentioning

confidence: 70%

Eplerenone enhances cardioprotective effects of standard heart failure therapy through matricellular proteins in hypertensive heart failure

Muñoz-Pacheco

Ortega‐Hernández²,

Caro-Vadillo³

et al. 2013

Journal of Hypertension

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Section: Discusionmentioning

confidence: 70%

Eplerenone enhances cardioprotective effects of standard heart failure therapy through matricellular proteins in hypertensive heart failure

Muñoz-Pacheco

Ortega‐Hernández²,

Caro-Vadillo³

et al. 2013

Journal of Hypertension

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“…Moreover, in an attempt to identify new predictive biomarkers for patients with myocardial infarction Devaux and colleagues found that the levels of TSP-1 mRNA expression in whole blood cells from patients with acute myocardial infarction predicted functional deterioration (113). In contrast, in end-stage heart failure patients, myocardial TSP-1 levels were decreased (32), perhaps reflecting the transient nature of TSP upregulation following cardiac injury. Intense upregulation of TSP-1 has also been reported in human cardiac allograft vasculopathy (508).…”

Section: The Matricellular Proteins Key Modulators Of Cell:cellmentioning

confidence: 99%

Matricellular Proteins in Cardiac Adaptation and Disease

Frangogiannis

2012

Physiological Reviews

384

375

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The term matricellular proteins describes a family of structurally unrelated extracellular macromolecules that, unlike structural matrix proteins, do not play a primary role in tissue architecture, but are induced following injury and modulate cell-cell and cell-matrix interactions. When released to the matrix, matricellular proteins associate with growth factors, cytokines, and other bioactive effectors and bind to cell surface receptors transducing signaling cascades. Matricellular proteins are upregulated in the injured and remodeling heart and play an important role in regulation of inflammatory, reparative, fibrotic and angiogenic pathways. Thrombospondin (TSP)-1, -2, and -4 as well as tenascin-C and -X secreted protein acidic and rich in cysteine (SPARC), osteopontin, periostin, and members of the CCN family (including CCN1 and CCN2/connective tissue growth factor) are involved in a variety of cardiac pathophysiological conditions, including myocardial infarction, cardiac hypertrophy and fibrosis, aging-associated myocardial remodeling, myocarditis, diabetic cardiomyopathy, and valvular disease. This review discusses the properties and characteristics of the matricellular proteins and presents our current knowledge on their role in cardiac adaptation and disease. Understanding the role of matricellular proteins in myocardial pathophysiology and identification of the functional domains responsible for their actions may lead to design of peptides with therapeutic potential for patients with heart disease.

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“…Interestingly, the predictive value of plasma TSP1 in this study was greater than both brain natriuretic peptide and troponin T (Devaux et al 2010). Conversely, TSP1 mRNA levels were decreased in biopsy samples from patients with end-stage LVF (Batlle et al 2009). One explanation for this may be that a compensatory response was at play.…”

Section: The Cd47-tsp1 Signaling Axis In Human Cvdmentioning

confidence: 99%

Thrombospondin-1 and CD47 regulation of cardiac, pulmonary and vascular responses in health and disease

et al. 2014

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Cardiovascular homeostasis and health is maintained through the balanced interactions of cardiac generated blood flow and cross-talk between the cellular components that comprise blood vessels. Central to this cross-talk is endothelial generated nitric oxide (NO) that stimulates relaxation of the contractile vascular smooth muscle (VSMC) layer of blood vessels. In cardiovascular disease this balanced interaction is disrupted and NO signaling lost. Work over the last several years indicates regulation of NO is much more complex than previously believed. It is now apparent the secreted protein thrombospondin-1 (TSP1), that is upregulated in cardiovascular disease and animal models of the same, on activating cell surface receptor CD47, redundantly inhibits NO production and NO signaling. This inhibitory event has implications for baseline and disease-related responses mediated by NO. Further work has identified that TSP1-CD47 signaling stimulates enzymatic reactive oxygen species (ROS) production to further limit blood flow and promote vascular disease. Herein consideration is given to the most recent discoveries in this regard which identify the TSP1-CD47 axis as a major proximate governor of cardiovascular health.

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Decreased Expression of Thrombospondin-1 in Failing Hearts May Favor Ventricular Remodeling

Cited by 21 publications

References 10 publications

Eplerenone enhances cardioprotective effects of standard heart failure therapy through matricellular proteins in hypertensive heart failure

Eplerenone enhances cardioprotective effects of standard heart failure therapy through matricellular proteins in hypertensive heart failure

Matricellular Proteins in Cardiac Adaptation and Disease

Thrombospondin-1 and CD47 regulation of cardiac, pulmonary and vascular responses in health and disease

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