Role of mast cells and their mediators in failing myocardium under mechanical ventricular support

Akgül, Ahmet; Skrabal, Christian; Thompson, Larry O.; Loebe, Matthias; Lafuente, Javier; Noon, George P.; Youker, Keith A.

doi:10.1016/j.healun.2003.06.006

Cited by 56 publications

(44 citation statements)

References 33 publications

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“…Second, the increased number of macrophages and also the presence of lymphocytes can be regarded as low grade inflammation (35) and may be associated with increased fibrosis through activation of mediators of inflammation such as TGF-beta (35,36). Third, mast cells, which were elevated in the Dex-group, can stimulate collagen expression by heart fibroblasts, by releasing its fibrogenic protease chymase, which can release TGF-beta and activate angiotensin II (36). Fourth, relative ischemia possibly induced by a lower capillary density (not determined in this study) may play a role.…”

Section: Discussionmentioning

confidence: 99%

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment: Studies in 4-, 8-, and 50-Week-Old Rats

et al. 2009

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Dexamethasone (Dex), for prevention of chronic lung disease in preterm infants, showed potential negative long-term effects. Studies regarding long-term cardiovascular effects are lacking. We investigated possible histopathological myocardial changes after neonatal Dex in the young and adult rat heart. Rats were treated with Dex on d 1, 2, and 3 (0.5, 0.3, and 0.1 mg/kg) of life. Control-pups received saline. At 4, 8, and 50 wk after birth rats were killed and anatomic data collected. Heart tissue was stained with hematoxylin and eosin, Cadherin-periodic acid schiff, and sirius red for cardiomyocyte morphometry and collagen determination. Presence of macrophages and mast cells was analyzed. Cardiomyocyte length of the Dex-treated rats was increased in all three age groups, whereas ventricular weight was reduced. Cardiomyocyte volumes were increased at 50 wk indicating cellular hypertrophy. Collagen content gradually increased with age and was 62% higher in Dex rats at 50 wk. Macrophage focus score and mast cell count were also higher. Neonatal Dex affects normal heart growth resulting in cellular hypertrophy and increased collagen deposition in the adult rat heart. Because previous studies in rats showed premature death, suggesting cardiac failure, cardiovascular follow-up of preterm infants treated with glucocorticoids should be considered. (Pediatr Res 66: 74-79, 2009)

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Section: Discussionmentioning

confidence: 99%

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment: Studies in 4-, 8-, and 50-Week-Old Rats

et al. 2009

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“…Conflicting changes in collagen content after LVAD support have been reported. Some groups report a decrease 9,[39][40][41] in the collagen content, whereas others report an increase. [42][43][44] The reasons for these differing responses, although still unclear, may be related to differences in the causes of HF, duration of unloading, 43,45 use of pharmacological therapy, and whether there is myocardial recovery.…”

Section: The Matrixmentioning

confidence: 99%

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Birks

2013

Circulation Research

106

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Abstract-Heart failure is associated with remodeling that consists of adverse cellular, structural, and functional changes in the myocardium. Until recently, this was thought to be unidirectional, progressive, and irreversible. However, irreversibility has been shown to be incorrect because complete or partial reversal can occur that can be marked after myocardial unloading with a left ventricular assist device (LVAD). Patients with chronic advanced heart failure can show near-normalization of nearly all structural abnormalities of the myocardium or reverse remodeling after LVAD support. However, reverse remodeling does not always equate with clinical recovery. The molecular changes occurring after LVAD support are reviewed, both those demonstrated with LVAD unloading alone in patients bridged to transplantation and those occurring in the myocardium of patients who have recovered enough myocardial function to have the device removed. Reverse remodeling may be attributable to a reversal of the pathological mechanisms that occur in remodeling or the generation of new pathways. A reduction in cell size occurs after LVAD unloading, which does not necessarily correlate with improved cardiac function. However, some of the changes in both the cardiac myocyte and the matrix after LVAD support are specific to myocardial recovery. In the myocyte, increases in the cytoskeletal proteins and improvements in the Ca 2+ handling pathway seem to be specifically associated with myocardial recovery. Changes in the matrix are complex, but excessive scarring appears to limit the ability for recovery, and the degree of fibrosis in the myocardium at the time of implantation may predict the ability to recover. (Circ Res. 2013;113:777-791.)

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“…On the contrary, another report alerts the occurrence of phenotypic shift in mast cells of DCM hearts with long-term mechanical support, 26) by which the fibrogenic content of mast cells was reportedly reduced. It may explain the healing property of mast cells in the chronic stage.…”

Section: )mentioning

confidence: 99%

Involvement of Mast Cells in the Development of Fibrosis in Rats with Postmyocarditis Dilated Cardiomyopathy

Selvaraj

Watanabe

et al. 2005

Biological & Pharmaceutical Bulletin

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Role of mast cells and their mediators in failing myocardium under mechanical ventricular support

Cited by 56 publications

References 33 publications

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment: Studies in 4-, 8-, and 50-Week-Old Rats

Histopathological Changes of the Heart After Neonatal Dexamethasone Treatment: Studies in 4-, 8-, and 50-Week-Old Rats

Molecular Changes After Left Ventricular Assist Device Support for Heart Failure

Involvement of Mast Cells in the Development of Fibrosis in Rats with Postmyocarditis Dilated Cardiomyopathy

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