The spatial pattern of coronary capillaries in patients with dilated, ischemic, or inflammatory cardiomyopathy

Karch, Rudolf; Neumann, Friederike; Ullrich, Robert C.; Neumüller, Josef; Podesser, Bruno K.; Neumann, Martin; Schreiner, Wolfgang

doi:10.1016/j.carpath.2005.03.003

Cited by 56 publications

(45 citation statements)

References 33 publications

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“…Furthermore, analyses of autopsy samples reveals that patients with end-stage heart failure, due to ischemic, inflammatory or idiopathic dilated cardiomyopathy, exhibit diminished densities and irregular patterns of myocardial capillaries [37] Indeed, agents that promote angiogenesis have been shown to be beneficial for cardiac remodeling after chronic myocardial ischemia [38][39][40]. In this study, the greater impaired LV function in adiponectin KO mice was accompanied by greater reductions in capillary density, whereas adenovirusmediated overexpression of adiponectin maintained capillary density in the infarct border zone.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Shibata

Izumiya

Sato

et al. 2007

Journal of Molecular and Cellular Cardiology

194

142

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Section: Discussionmentioning

confidence: 99%

Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Shibata

Izumiya

Sato

et al. 2007

Journal of Molecular and Cellular Cardiology

194

142

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“…These studies also suggest that impaired expression of myocardial angiogenic growth factors in the pathological phase of pressure overload-induced cardiac hypertrophy results in vascular rarefaction and has a causative role in the development of contractile dysfunction. Consistent with this hypothesis, clinical dilated cardiomyopathy is associated with an irregular capillary pattern and a reduction in overall capillary density (9,10). Thus the balance between growth and angiogenesis in the heart is one of the determinants of whether the hypertrophy is physiological/adaptive or pathological/ maladaptive, and impaired angiogenesis during sustained growth stimuli is critical for the progression from adaptive to maladaptive cardiac hypertrophy (11).…”

mentioning

confidence: 82%

Cardiac growth and angiogenesis coordinated by intertissue interactions

Walsh¹,

Shiojima²

2007

J. Clin. Invest.

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“…For example, in human heart diseases such as aortic stenosis, dilated cardiomyopathy, and ischemic cardiomyopathy, there is a significant decrease in myocardial capillary density (Rakusan et al 1992;Karch et al 2005). Short-term Akt activation in inducible Akt1 TG mice induces physiological hypertrophy with maintained vascular density .…”

Section: Akt Signaling and Coronary Angiogenesismentioning

confidence: 99%

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

Shiojima¹,

Walsh²

2006

Genes Dev.

323

260

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Postnatal growth of the heart is primarily achieved through hypertrophy of individual myocytes. Cardiac growth observed in athletes represents adaptive or physiological hypertrophy, whereas cardiac growth observed in patients with hypertension or valvular heart diseases is called maladaptive or pathological hypertrophy. These two types of hypertrophy are morphologically, functionally, and molecularly distinct from each other. The serine/threonine protein kinase Akt is activated by various extracellular stimuli in a phosphatidylinositol-3 kinasedependent manner and regulates multiple aspects of cellular functions including survival, growth and metabolism. In this review we will discuss the role of the Akt signaling pathway in the heart, focusing on the regulation of cardiac growth, contractile function, and coronary angiogenesis. How this signaling pathway contributes to the development of physiological/pathological hypertrophy and heart failure will also be discussed.Growth of the heart during embryonic development occurs primarily through proliferation of cardiac myocytes. However, cardiac myocytes withdraw from the cell cycle soon after birth, and subsequent growth of the heart during postnatal development is achieved predominantly through hypertrophy rather than hyperplasia of individual myocytes (Pasumarthi and Field 2002;Olson and Schneider 2003). In fact, there is almost a threefold increase in cardiac myocyte diameter in humans during development from infants to adults (Hudlicka and Brown 1996). Cardiac growth during normal postnatal development or the hypertrophy observed in trained athletes is referred to as "physiological," and it is characterized by normal or enhanced contractile function and normal architecture and organization of cardiac structure (Richey and Brown 1998). On the other hand, cardiac hypertrophy is also observed in patients with pathological conditions such as hypertension, myocardial infarction, and valvular heart diseases. This type of cardiac growth is called "pathological" hypertrophy, and is frequently associated with contractile dysfunction, interstitial fibrosis, and re-expression of fetal-type cardiac genes such as atrial natriuretic peptide and ␤-myosin heavy chain (Molkentin and Dorn 2001;Frey and Olson 2003). These data indicate that pathological cardiac hypertrophy is morphologically and molecularly distinct from physiological cardiac hypertrophy. The pathological form of cardiac hypertrophy is initially recognized as an adaptive response to increased external load, because increased wall stress induced by overload is attenuated by the increase in wall thickness. However, increased cardiac mass is clinically associated with increased morbidity and mortality (Levy et al. 1990), and a sustained overload eventually leads to contractile dysfunction and heart failure through poorly understood mechanisms (Molkentin and Dorn 2001;Frey and Olson 2003). In addition, hypertrophy of individual myocyte is a common feature of failing myocardium (Gerdes et al. 1992). Thus, pathological ...

show abstract

The spatial pattern of coronary capillaries in patients with dilated, ischemic, or inflammatory cardiomyopathy

Cited by 56 publications

References 33 publications

Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Cardiac growth and angiogenesis coordinated by intertissue interactions

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

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