Fibroblast‐mediated intercellular crosstalk in the healthy and diseased heart

Nicin, Luka; Wagner, Jasmin; Luxán, Guillermo; Dimmeler, Stefanie

doi:10.1002/1873-3468.14234

Cited by 42 publications

(24 citation statements)

References 150 publications

(208 reference statements)

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“…In support of this, Fgf2 mRNA expression was significantly upregulated in hearts of mice treated with AngII, and the increase in expression was reduced in mouse hearts with cardiomyocyte BRAF knockout (Figure 3D). This is consistent with the concept of cross-talk between cardiomyocytes and the non-myocytes in the heart [36].…”

Section: Cardiomyocyte Braf Is Required For Cardiac Adaptation To Hyp...supporting

confidence: 91%

Cardiomyocyte BRAF is a key signalling intermediate in cardiac hypertrophy in mice

Alharbi

Hardyman

Cull

et al. 2022

Preprint

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Cardiac hypertrophy is necessary for the heart to accommodate an increase in workload. Physiological, compensated hypertrophy (e.g. with exercise) is reversible and largely due to cardiomyocyte hypertrophy. Pathological hypertrophy (e.g. with hypertension) is associated with additional features including increased fibrosis and can lead to heart failure. RAF kinases (ARAF/BRAF/RAF1) integrate signals into the ERK1/2 cascade, a pathway implicated in cardiac hypertrophy, and activation of BRAF in cardiomyocytes promotes compensated hypertrophy. Here, we used mice with tamoxifen-inducible cardiomyocyte-specific BRAF knockout (CM-BRAFKO) to assess the role of BRAF in hypertension-associated cardiac hypertrophy induced by angiotensin II (AngII; 0.8 mg/kg/d, 7 d) and physiological hypertrophy induced by phenylephrine (40 mg/kg/d, 7 d). Cardiac dimensions/function were assessed by echocardiography with histological assessment of cellular changes. AngII promoted cardiomyocyte hypertrophy and increased fibrosis within the myocardium (interstitial) and around the arterioles (perivascular) in male mice; cardiomyocyte hypertrophy and interstitial (but not perivascular) fibrosis were inhibited in mice with CM-BRAFKO. Phenylephrine had a limited effect on fibrosis, but promoted cardiomyocyte hypertrophy and increased contractility in male mice; cardiomyocyte hypertrophy was unaffected in mice with CM-BRAFKO, but the increase in contractility was suppressed and fibrosis increased. Phenylephrine induced a modest hypertrophic response in female mice and, in contrast to the males, tamoxifen-induced loss of cardiomyocyte BRAF reduced cardiomyocyte size, had no effect on fibrosis and increased contractility. The data identify BRAF as a key signalling intermediate in both physiological and pathological hypertrophy in male mice, and highlight the need for independent assessment of gene function in females.

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Section: Cardiomyocyte Braf Is Required For Cardiac Adaptation To Hyp...supporting

confidence: 91%

Cardiomyocyte BRAF is a key signalling intermediate in cardiac hypertrophy in mice

Alharbi

Hardyman

Cull

et al. 2022

Preprint

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“…Among the three isoforms, TGF-β1 is predominant. It is crucial in pathological fibrosis and is produced by various cells, including immune cells, endothelial cells, cardiomyocytes, and activated fibroblasts [ 111 , 112 ]. TGF-β1 is initially secreted as an inactive complex with latent TGF-β-binding proteins and TGF-β pro-peptides.…”

Section: Signaling Pathways In Cardiac Fibrosismentioning

confidence: 99%

The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress

Maruyama

Imanaka‐Yoshida

2022

IJMS

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Fibrosis is defined as the excessive deposition of extracellular matrix (ECM) proteins in the interstitium. It is an essential pathological response to chronic inflammation. ECM protein deposition is initially protective and is critical for wound healing and tissue regeneration. However, pathological cardiac remodeling in excessive and continuous tissue damage with subsequent ECM deposition results in a distorted organ architecture and significantly impacts cardiac function. In this review, we summarized and discussed the histologic features of cardiac fibrosis with the signaling factors that control it. We evaluated the origin and characteristic markers of cardiac fibroblasts. We also discussed lymphatic vessels, which have become more important in recent years to improve cardiac fibrosis.

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“…Andreas Herrlich’s review ‘Interorgan crosstalk mechanisms in disease: the case of acute kidney injury‐induced remote lung injury’ [41] highlights the role of kidney‐released mediators that cause lung endothelial leakage, lung edema, lung inflammation, and respiratory failure as one important example of such clinically important crosstalk. Luka Nicin, Julian U G Wagner, Guillermo Luxán and Stefanie Dimmeler’s review ‘Fibroblast‐mediated intercellular crosstalk in the healthy and diseased heart’ [42] reports current knowledge of cellular interactions in the healthy, diseased, and aging heart and their potential relevance for interorgan crosstalk.…”

mentioning

confidence: 99%