1. Under biomechanical overload, cardiac fibroblasts and myocytes respond to an altered environment via multiple mechanisms including integrin-extracellular matrix interactions and renin-angiotensin-aldosterone axis activation. Cardiac fibroblasts increase synthesis of matrix proteins and secrete a variety of paracrine factors that can stimulate myocyte hypertrophy. Cardiac myocytes similarly respond by secreting a conglomerate of factors. Hormones such as TGFβ1, FGF2, and the IL-6 family members LIF and CT-1 have all been implicated in this bidirectional fibroblast-myocyte hormonal crosstalk.

2.The IL33/ST2 system in the heart. The IL-33/ST2 system is a recently described cardiac fibroblast-myocyte signaling system. This signaling pathway serves an antihypertrophic and cardioprotective mechanism in the face of biomechanical overload. IL-33 is produced by mechanically loaded cardiac fibroblasts and is possibly inactivated by caspases. Extracellular IL-33 may bind to a soluble “decoy” form of its receptor, sST2, and be removed from the biologically available pool, or it may bind a transmembrane form, ST2L, on the surface of cardiac myocytes. In the face of prohypertrophic stimuli in vitro or pressure overload in vivo, IL-33 appears to confer antihypertrophic and antifibrotic properties to the myocardium.



  1. Do you know about the Fibroblast growth factors (FGF)?
    A major group of molecules with key roles in the regulation of cell proliferation and differentiation is growth factors. Several fibroblast growth factors (FGFs), and in particular FGF8 and FGF3, are expressed in the anterior neural ridge, the midbrain-hindbrain barrier and the prospective rhombomere 4 of the hindbrain early in development (Mason, 2007).
    FGF expression profile increases in complexity during development. FGF activity is critical not only for the patterning of the nervous system but also for other functions, such as the FGF8-dependent survival of cells in the forebrain (Storm et al., 2003) and the midbrain-hindbrain region (Chi et al., 2003). Moreover, FGF-2 (or bFGF) is a mitogen widely used in vitro, as it is essential for keeping precursors of the embryonic telencephalon and neural tube in a progenitor state and bFGF deficient mice have small brains due to a marked decrease in the NSC/precursor population .

    FGF (Fibroblast growth factors) play an important role in embryonic stem cell behavior as it is supported by the reported expression of all FGF receptors (FGFRs) in vivo.
    FGFR4 was shown to be highly expressed in neural tube neuroepithelial cells , while zebrafish dorsal telencephalon neuroepithelial cells were found to express mostly FGFR1 and 3 with these receptors being pivotal for self-renewing symmetric cell divisions.
    Now isn’t that interesting?


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