Osteocrin was originally classified as a muscular and bone secretory protein with the ability to modulate bone growth through osteoblast activity, yet it shares a similar sequence to the family of natriuretic peptides (NPs). Despite their sequence homology, it is yet unknown whether osteocrin exhibits similar properties to NPs. However, recent work has shown that osteocrin can limit C-type NPs and more definitively, that a transgenic osteocrin mouse strain exhibited improved outcomes and alleviated echocardiographic parameters, after myocardial infarction (MI).
With previous evidence showing improved prognosis and cardiac function in osteocrin-overexpressing mice post-MI, we hypothesize that circulating osteocrin levels in chronic heart failure patients could track with echocardiographic indices and other heart failure (HF) biomarkers of interest.
Eighty-seven symptomatic chronic HF subjects with LVEF ≤35% underwent detailed echocardiographic evaluation and measurements of plasma NPs and osteocrin by ELISA assay, with long-term follow-up for all-cause mortality, transplantation, or mechanical circulatory support.
In our study cohort (mean age 57 years, 72% male, 44% ischemic), median plasma osteocrin level was 198.3 (IQR 131.5, 386.3) ng/L. Plasma osteocrin levels did not track with demographics, comorbidities, medications, or laboratory values including ANP and BNP. Furthermore, osteocrin did not correlate to major echocardiographic indices (Table) or long-term adverse clinical outcomes.
Although osteocrin shows similarity to NPs and has been shown to exert cardioprotective effects in mice after cardiac insult, we did not observe any relationship between circulating osteocrin levels and clinical or echocardiographic parameters in chronic HFrEF patients.
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