How cardiomyocytes sense pathophysiological stresses for cardiac remodeling

Haque, Zaffar K.; Wang, Dazhi

doi:10.1007/s00018-016-2373-0

Cited by 54 publications

(37 citation statements)

References 158 publications

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“…Consistent with the observation that adverse remodeling selectively occurs in adult DCM, genes previously associated with pathological cardiomyocyte hypertrophy in humans and animal models (Nppa, Myh7, Mybpc3, Actc1, Tpm1, Des, Lmna, Myl3, Mylk3, Pln, Gdf15, and Mef2) (29)(30)(31)(32) were upregulated in adult compared with pediatric DCM. Myh6, a gene that is known to decrease with pathological cardiomyocyte hypertrophy, was downregulated in adult compared with pediatric DCM ( Figure 6D).…”

Section: D-f)supporting

confidence: 79%

Pediatric and adult dilated cardiomyopathy represent distinct pathological entities

Patel¹,

Mohan²,

Schneider³

et al. 2017

JCI Insight

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Section: D-f)supporting

confidence: 79%

Pediatric and adult dilated cardiomyopathy represent distinct pathological entities

Patel¹,

Mohan²,

Schneider³

et al. 2017

JCI Insight

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“…Physiologic and pathophysiologic stimuli act upon the cell membrane and work their way through various cascades to mediate gene expression, translational control and protein levels (Haque and Wang, 2017). As expected, pressure overload was associated with profound changes in the composition of the extracellular matrix (ECM), which…”

Section: Discussionmentioning

confidence: 80%

A multi-network comparative analysis of transcriptome and translatome in cardiac remodeling

Boileau

Doroudgar

Riechert

et al. 2020

Preprint

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Our understanding of the transition from physiological to pathological cardiac hypertrophy remains elusive and largely based on reductionist hypotheses. Here, we profiled the translatomes of 15 mouse hearts to provide a molecular blueprint of altered gene networks in early cardiac remodeling. Using co-expression analysis, we reveal how sub-networks are orchestrated into functional modules associated with pathological phenotypes. We show how transcriptome networks are only partially reproducible at the translatome level. We find unappreciated hub genes and genes in the transcriptional network that were rewired in the translational network, and associated with semantically different subsets of enriched functional terms, providing novel insights into the complexity of the organization of in vivo cardiac regulatory networks.

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“…The mechanisms underlying the cardio-protective effects of Andr are not clear. In human patients with heart failure, MAPK signaling proteins have been reported to be hyperactive ( Haque and Wang, 2017 ). Under physiological conditions MAPKs regulate cell proliferation and differentiation, whereas under pathological conditions, activated MAPKs induce the hypertrophic gene transcription ( Liu and Molkentin, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Andrographolide Protects against Aortic Banding-Induced Experimental Cardiac Hypertrophy by Inhibiting MAPKs Signaling

Ni²,

Zhang³

et al. 2017

Front. Pharmacol.

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Despite therapeutic advances, heart failure-related mortality rates remain high. Therefore, understanding the pathophysiological mechanisms involved in the remodeling process is crucial for the development of new therapeutic strategies. Andrographolide (Andr), a botanical compound, has potent cardio-protective effects due to its ability to inhibit mitogen-activated protein kinases (MAPKs). Andr has also been shown to inhibit inflammation and apoptosis, which are factors related to cardiac hypertrophy. Our aim was to evaluate the effects of Andr on cardiac hypertrophy and MAPKs activation. Thus, mice were subjected to aortic banding (AB) with/without Andr administration (25 mg/kg/day, orally). Cardiac function was accessed by echocardiography and hemodynamic parameters. Our results showed that Andr administration for 7 weeks decreased cardiac dysfunction and attenuated cardiac hypertrophy and fibrosis in AB mice. Andr treatment induced a strong reduction in the transcription of both hypertrophy (ANP, BNP, and β-MHC) and fibrosis related genes (collagen I, collagen III, CTGF, and TGFβ). In addition, cardiomyocytes treated with Andr showed a reduced hypertrophic response to angiotensin II. Andr significantly inhibited MAPKs activation in both mouse hearts and cardiomyocytes. Treatment with a combination of MAPKs activators abolished the protective effects of Andr in cardiomyocytes. Furthermore, we found that Andr also inhibited the activation of cardiac fibroblasts via the MAPKs pathway, which was confirmed by the application of MAPKs inhibitors. In conclusion, Andr was found to confer a protective effect against experimental cardiac hypertrophy in mice, suggesting its potential as a novel therapeutic drug for pathological cardiac hypertrophy.

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How cardiomyocytes sense pathophysiological stresses for cardiac remodeling

Cited by 54 publications

References 158 publications

Pediatric and adult dilated cardiomyopathy represent distinct pathological entities

Pediatric and adult dilated cardiomyopathy represent distinct pathological entities

A multi-network comparative analysis of transcriptome and translatome in cardiac remodeling

Andrographolide Protects against Aortic Banding-Induced Experimental Cardiac Hypertrophy by Inhibiting MAPKs Signaling

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