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Editorial
. 2017 Apr 7:4:26.
doi: 10.21037/sci.2017.03.05. eCollection 2017.

Role of "osteogenic" cardiac fibroblasts in pathological heart calcification

Hong Zhan  1 , Toru Suzuki  2   3
Affiliations
Editorial

Role of "osteogenic" cardiac fibroblasts in pathological heart calcification

Hong Zhan et al. Stem Cell Investig. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Cardiac fibroblasts adopt osteogenic cell-like fates, and the CF and the ENPP1-PPi-Pi axis can be targeted to decrease pathological cardiac calcification and improve cardiac function. Induction of expression of stable canonical osteoblast markers (i.e., Runx2, osteocalcin) were confirmed in cardiac fibroblasts following osteogenic differentiation (blue arrow) or cardiac fibroblasts (CFs) isolated from multiple models of myocardial calcification induced after a variety of injuries (high-dose systemic steroids, cyro and ischemic injury) (red arrow). Cell transplantation experiments where CFs harvested following explant culture of calcified or uninjured myocardium of C3H mice were injected into subcutaneous pockets of another host showed a direct role of CFs isolated from calcific heart lesions in mediating ectopic soft tissue calcification (red arrow). Expression of ENPP1 and Pi, and formation of calcium hydroxyapatite were markedly increased in calcified regions of injured C3H mouse hearts. Pre-treatment with small molecules (SYL-001 or ARL67156) that inhibit ENPP1, or inhibitors of bone mineralization, bisphosphonates (e.g., etidronate), that inhibit the function of ENPP1-PPi-Pi axis followed by injury, led to significantly decreased cardiac calcification and improved post-injury cardiac function.
See this image and copyright information in PMC

Comment on

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