Disruptions and detours in the myocardial matrix highway and heart failure

Deschamps, Anne M.; Spinale, Francis G.

doi:10.1007/s11897-005-0002-6

Cited by 17 publications

(8 citation statements)

References 79 publications

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“…Recent studies have demonstrated that fibroblasts have other critical functions other than ECM synthesis, deposition and remodeling 173 . Cardiac fibroblasts have a high membrane resistance, which makes them good conductors.…”

Section: Cardiac Fibroblasts and Electrical Signalingmentioning

confidence: 99%

Cardiac Fibroblast

Souders

Bowers

Baudino

2009

Circulation Research

835

481

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The permanent cellular constituents of the heart include cardiac fibroblasts, myocytes, endothelial cells and vascular smooth muscle cells. Previous studies have demonstrated that there are undulating changes in cardiac cell populations during embryonic development, through neonatal development and into the adult. Transient cell populations include lymphocytes, mast cells and macrophages, which can interact with these permanent cell types to affect cardiac function. It has also been observed that there are marked differences in the makeup of the cardiac cell populations depending on the species, which may be important when examining myocardial remodeling. Current dogma states that the fibroblast makes up the largest cell population of the heart; however, this appears to vary for different species, especially mice. Cardiac fibroblasts play a critical role in maintaining normal cardiac function, as well as in cardiac remodeling during pathological conditions such as myocardial infarct and hypertension. These cells have numerous functions, including synthesis and deposition of extracellular matrix, cell-cell communication with myocytes, cell-cell signaling with other fibroblasts, as well as with endothelial cells. These contacts affect the electrophysiological properties, secretion of growth factors and cytokines, as well as potentiating blood vessel formation. While a plethora of information is known about several of these processes, relatively little is understood about fibroblasts and their role in angiogenesis during development or cardiac remodeling. In this review we provide insight into the various properties of cardiac fibroblasts that helps illustrate their importance in maintaining proper cardiac function, as well as their critical role in the remodeling heart.

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Section: Cardiac Fibroblasts and Electrical Signalingmentioning

confidence: 99%

Cardiac Fibroblast

Souders

Bowers

Baudino

2009

Circulation Research

835

481

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“…Cardiac diseases (CD) frequently progress into heart failure. Progression of CD may result from multiple myocardial remodeling events, initially as beneficial adaptive changes, but eventually resulting in dysregulation of collagen synthesis and heart failure . Chronic heart failure is associated with enhanced catabolic metabolism finally resulting in overall weight loss and cardiac cachexia …”

mentioning

confidence: 99%

“…Progression of CD may result from multiple myocardial remodeling events, initially as beneficial adaptive changes, but eventually resulting in dysregulation of collagen synthesis and heart failure. [1][2][3] Chronic heart failure is associated with enhanced catabolic metabolism finally resulting in overall weight loss and cardiac cachexia. 4 Leptin, an adipokine, influences body weight and regulates energy homoeostasis by decreasing appetite and increasing basal metabolic rate.…”

mentioning

confidence: 99%

Leptin Expression in Dogs with Cardiac Disease and Congestive Heart Failure

Fonfara

Hetzel

Tew

et al. 2011

Veterinary Internal Medicne

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Background: Leptin belongs to the group of adipokines and has recently attracted attention because of its effects on the cardiovascular system. Increased leptin concentrations are reported in obese dogs but its role in cardiac disease (CD) is not known. Therefore, we investigated leptin expression in blood samples from dogs with congestive heart failure (CHF), and from myocardial samples of dogs with CDs.Methods: Leptin mRNA was analyzed from blood samples of 8 dogs presented for cardiac screening in which no abnormalities were detected and 8 dogs in CHF. In addition, myocardial samples (interventricular septum, right and left atria, and ventricles) of 10 dogs with no cardiac abnormalities (controls), 7 dogs with acquired and 3 dogs with congenital CDs were investigated using real-time polymerase chain reaction (PCR).Results: Dogs with CHF had significantly higher blood concentrations of leptin mRNA than dogs without CD (P = .013). Myocardial leptin expression was significantly increased in acquired (P = .035) and decreased in congenital CD (P = .016) in comparison to controls. Dogs in heart failure stage D showed higher myocardial leptin concentrations than dogs in stage C3 and B (P = .031). Differences according to myocardial region (P < .05) were detected and higher leptin concentrations were present in the atria in comparison to the ventricles in dogs with CD (P = .005). Comparing male and female dogs with CD revealed higher leptin concentrations in female dogs (P = .001).Conclusions: These results indicate leptin mRNA concentrations vary with CD, severity of CD, myocardial region, and possibly sex. Therefore, leptin might play a role in canine CD.

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“…This study confirmed that chronic hypoxia breaks the delicate balance of proteolytic and anti-proteolytic forces during lung development, which accounts for several pulmonary pathologies, including pulmonary fibrosis. The TIMP-1:MMP-1 ratio was also remarkably increased in patients with severe left ventricular hypertrophy, showing that the interaction of TIMP-1 with another MMP besides MMP-9 also has a significant role in the pathophysiological remodeling [80]. The disruption of fine dynamics of MMP–TIMPs by acute hypoxia is also supported by studies using a neonatal hypoxic ischemia (HI) model.…”

Section: The Role Of Mmps and Timps In Hypoxia-induced Abnormal Heartmentioning

confidence: 99%

Fetal hypoxia and programming of matrix metalloproteinases

Tong

Zhang

2012

Drug Discovery Today

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Fetal hypoxia adversely affects the brain and heart development, yet the mechanisms responsible remain elusive. Recent studies indicate an important role of the extracellular matrix in fetal development and tissue remodeling. The matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of metalloproteinases (TIMPs) have been implicated in a variety of physiological and pathological processes in the cardiovascular and central nervous systems. This review summarizes current knowledge of the mechanisms by which fetal hypoxia induces the imbalance of MMPs, TIMPs and collagen expression patterns, resulting in growth restriction and aberrant tissue remodeling in the developing heart and brain. Collectively, this information could lead to the development of preventive diagnoses and therapeutic strategies in the fetal programming of cardiovascular and neurological disorders.

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Disruptions and detours in the myocardial matrix highway and heart failure

Cited by 17 publications

References 79 publications

Cardiac Fibroblast

Cardiac Fibroblast

Leptin Expression in Dogs with Cardiac Disease and Congestive Heart Failure

Fetal hypoxia and programming of matrix metalloproteinases

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