Plasma FGF23 does not rise during physical exercise as a physiological model of sympathetic activation
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After the failure of conventional pharmacological strategies for cardiovascular prevention in chronic kidney disease (CKD) [1, 2], the phosphaturic hormone FGF23 emerged as a promising therapeutic target for novel cardioprotective interventions in CKD [3, 4]. Elevated FGF23 has been found associated with cardiovascular disease both in experimental studies and in non-interventional human cohort studies . Nevertheless, our understanding of the physiological regulation of FGF23 is incomplete, and its deciphering appears mandatory.
The rise of FGF23 which inevitably occurs during CKD progression cannot be fully explained by canonical pathways within the chronic kidney disease—mineral and bone disorders (CKD-MBD) spectrum . Instead, non-canonical factors may contribute to high plasma FGF23 in CKD patients. Recently, murine data suggested increased sympathetic activity to induce FGF23 synthesis .
However, the physiological relevance of such a rise of FGF23 caused by increased...
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