Myokardfibrose: ein kardiopathophysiologischer Januskopf

Maisch, Bernhard; Rupp, Heinz

doi:10.1007/s00059-006-2823-9

Cited by 12 publications

(2 citation statements)

References 27 publications

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“…Excessive fibrosis, as it occurs under conditions of chronic myocarditis, can be classified as either replacement fibrosis, when functional tissue is replaced by connective tissue, or as reactive fibrosis, which is part of an adaptive process [139]. In addition to collagen, tenascin C, and fibronectin, splice variants of these molecules are often part of the fibrotic tissue [140,141].…”

Section: Tgf--related Molecules In Myocarditismentioning

confidence: 99%

TGF-β and fibrosis in different organs — molecular pathway imprints

Pohlers

Brenmoehl

Löffler

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

557

436

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The action of transforming-growth-factor (TGF)-beta following inflammatory responses is characterized by increased production of extracellular matrix (ECM) components, as well as mesenchymal cell proliferation, migration, and accumulation. Thus, TGF-beta is important for the induction of fibrosis often associated with chronic phases of inflammatory diseases. This common feature of TGF-related pathologies is observed in many different organs. Therefore, in addition to the description of the common TGF-beta-pathway, this review focuses on TGF-beta-related pathogenetic effects in different pathologies/organs, i. e., arthritis, diabetic nephropathy, colitis/Crohn's disease, radiation-induced fibrosis, and myocarditis (including their similarities and dissimilarities). However, TGF-beta exhibits both exacerbating and ameliorating features, depending on the phase of disease and the site of action. Due to its central role in severe fibrotic diseases, TGF-beta nevertheless remains an attractive therapeutic target, if targeted locally and during the fibrotic phase of disease.

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Section: Tgf--related Molecules In Myocarditismentioning

confidence: 99%

TGF-β and fibrosis in different organs — molecular pathway imprints

Pohlers

Brenmoehl

Löffler

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

557

436

View full text Add to dashboard Cite

show abstract

“…For those features endomyocardial biopsy and their comprehensive work-up including PCR on cardiotropic agents is extremely helpful [48,66,67]. The metabolism of collagen, the matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) can be appreciated in [51]. Regression of fibrosis in dilated cardiomyopathy or in hypertensive heart muscle disease has been demonstrated by treatment with angiotensin converting enzyme (ACE) inhibitors, e.g.…”

Section: Role Of Endomyocardial Biopsymentioning

confidence: 99%

Diabetic cardiomyopathy—fact or fiction?

Maisch

Alter

Pankuweit

2011

Herz

141

139

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Epidemiologic as well as clinical studies confirm the close link between diabetes mellitus and heart failure. Diabetic cardiomyopathy (DCM) is still a poorly understood "entity", however, with several contributing pathogenetic factors which lead in different stages of diabetes to characteristic clinical phenotypes. Hyperglycemia with a shift from glucose metabolism to increased beta-oxidation and consecutive free fatty acid damage (lipotoxicity) to the myocardium, insulin resistance, renin-angiotensin-aldosterone system (RAAS) activation, altered calcium homeostasis and structural changes from the natural collagen network to a stiffer matrix due to advanced glycation endproduct (AGE) formation, hypertrophy and fibrosis contribute to the respective clinical phenotypes of DCM. We propose the following classification of cardiomyopathy in diabetic patients: a) Diastolic heart failure with normal ejection fraction (HFNEF) in diabetic patients often associated with hypertrophy without relevant hypertension. Relevant coronary artery disease (CAD), valvular disease and uncontrolled hypertension are not present. This is referred to as stage 1 DCM. b) Systolic and diastolic heart failure with dilatation and reduced ejection (HFREF) in diabetic patients excluding relevant CAD, valvular disease and uncontrolled hypertension as stage 2 DCM. c) Systolic and/or diastolic heart failure in diabetic patients with small vessel disease (microvascular disease) and/or microbial infection and/or inflammation and/or hypertension but without CAD as stage 3 DCM. d) If heart failure may also be attributed to infarction or ischemia and remodeling in addition to stage 3 DCM the term should be heart failure in diabetes or stage 4 DCM. These clinical phenotypes of diabetic cardiomyopathy can be separated by biomarkers, non-invasive (echocardiography, cardiac magnetic resonance imaging) and invasive imaging methods (levocardiography, coronary angiography) and further analysed by endomyocardial biopsy for concomitant viral infection. The role of specific diabetic drivers to the clinical phenotypes, to macro- and microangiopathy as well as accompanying risk factors or confounders, e.g. hypertension, autoimmune factors or inflammation with or without viral persistence, need to be identified in each individual patient separately. Thus hyperglycemia, hyperinsulinemia and insulin resistance as well as lipotoxicity by free fatty acids (FFAs) are the factors responsible for diabetic cardiomyopathy. In stage 1 and 2 DCM diabetic cardiomyopathy is clearly a fact. However, precise determination of to what degree the various underlying pathogenetic processes are responsible for the overall heart failure phenotype remains a fiction.

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Pathology of Mitral Stenosis

Warth

Herpel

2010

Cardiovascular Interventions in Clinical Practice

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Myokardfibrose: ein kardiopathophysiologischer Januskopf

Cited by 12 publications

References 27 publications

TGF-β and fibrosis in different organs — molecular pathway imprints

TGF-β and fibrosis in different organs — molecular pathway imprints

Diabetic cardiomyopathy—fact or fiction?

Pathology of Mitral Stenosis

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