Treatment of myocardial interstitial fibrosis in pathological myocardial hypertrophy

Figures

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  FIGURE 1. Major signalling pathways involved in the activation of cardiac fibroblasts. In response to increased mechanical stress and to cardiac injury, inflammatory signalling cascades (triggered by cytokines and chemokines), mechanosensitive mechanisms (mediated by integrins and ion channels), and neurohumoral pathways (such as renin-angiotensin-aldosterone system) can activate fibroblasts into extracellular matrix-synthesizing myofibroblasts. Among them, TGF-β is the main regulator of fibrogenesis through SMAD-dependent pathway and none-canonical signal cascade. Ang II also plays an important role in cardiac fibrosis, which activates profibrotic cascades, such as TGF- β/SMAD, ERK1/2, AKT and MAPK. AT1R, type 1 angiotensin II receptor; CCL2, CC- chemokine ligand 2; CCR, CC- chemokine receptor; ERK, extracellular-signal- regulated kinase; FAK, focal adhesion kinase; IL-11RA, IL-11 receptor subunit- α; MAPK, mitogen-activated protein kinase; MR, mineralocorticoid receptor; PI3K, phosphoinositide 3-kinase; RHOA, transforming protein RHOA; TAK1, TGFβ-activated kinase 1; TGFβR1, TGFβ receptor type 1.

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  FIGURE 2. The Process of Myocardial Interstitial Fibrosis in pathological myocardial hypertrophy. Steps in the process of myocardial interstitial fibrosis, including major mechanisms and consequences. MIF, myocardial interstitial fibrosis.

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  FIGURE 3. Adverse consequences of MIF. MIF, myocardial interstitial fibrosis.