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Bone
2017 ; 100
(?): 69-79
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Cardiac actions of fibroblast growth factor 23
#MMPMID27725315
Faul C
Bone
2017[Jul]; 100
(?): 69-79
PMID27725315
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Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell
proliferation and survival. Although cardiac myocytes are post-mitotic, they have
been shown to be able to respond to local and circulating FGFs. While precise
molecular mechanisms are not well characterized, some FGF family members have
been shown to induce cardiac remodeling under physiologic conditions by mediating
hypertrophic growth in cardiac myocytes and by promoting angiogenesis, both
events leading to increased cardiac function and output. This FGF-mediated
physiologic scenario might transition into a pathologic situation involving
cardiac cell death, fibrosis and inflammation, and eventually cardiac dysfunction
and heart failure. As discussed here, cardiac actions of FGFs - with the majority
of studies focusing on FGF2, FGF21 and FGF23 - and their specific FGF receptors
(FGFR) and precise target cell types within the heart, are currently under
experimental investigation. Especially cardiac effects of endocrine FGFs entered
center stage over the past five years, as they might provide communication routes
that couple metabolic mechanisms, such as bone-regulated phosphate homeostasis,
or metabolic stress, such as hyperphosphatemia associated with kidney injury,
with changes in cardiac structure and function. In this context, it has been
shown that elevated serum FGF23 can directly tackle cardiac myocytes via FGFR4
thereby contributing to cardiac hypertrophy in models of chronic kidney disease,
also called uremic cardiomyopathy. Precise characterization of FGFs and their
origin and regulation of expression, and even more importantly, the
identification of the FGFR isoforms that mediate their cardiac actions should
help to develop novel pharmacological interventions for heart failure, such as
FGFR4 inhibition to tackle uremic cardiomyopathy.
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