Abstract
Bone morphogenetic protein-7 is (BMP-7) is a potent anti-inflammatory growth factor belonging to the Transforming Growth Factor Beta (TGF-β) superfamily. It plays an important role in various biological processes, including embryogenesis, hematopoiesis, neurogenesis and skeletal morphogenesis. BMP-7 stimulates the target cells by binding to specific membrane-bound receptor BMPR 2 and transduces signals through mothers against decapentaplegic (Smads) and mitogen activated protein kinase (MAPK) pathways. To date, rhBMP-7 has been used clinically to induce the differentiation of mesenchymal stem cells bordering the bone fracture site into chondrocytes, osteoclasts, the formation of new bone via calcium deposition and to stimulate the repair of bone fracture. However, its use in cardiovascular diseases, such as atherosclerosis, myocardial infarction, and diabetic cardiomyopathy is currently being explored. More importantly, these cardiovascular diseases are associated with inflammation and infiltrated monocytes where BMP-7 has been demonstrated to be a key player in the differentiation of pro-inflammatory monocytes, or M1 macrophages, into anti-inflammatory M2 macrophages, which reduces developed cardiac dysfunction. Therefore, this review focuses on the molecular mechanisms of BMP-7 treatment in cardiovascular disease and its role as an anti-fibrotic, anti-apoptotic and anti-inflammatory growth factor, which emphasizes its potential therapeutic significance in heart diseases.
Highlights
In 1970, a physician named Marshall Urist coined the term bone morphogenetic protein (BMP)after demonstrating that these proteins play an important role in osteogenesis and bone formation.Thereafter, more than 20 BMPs have been identified and subdivided into the following four groups; (i)BMP-2/4, (ii) BMP-5/6/7/8a/8b, (iii) BMP-9/10, and (iv) BMP-12/13/14 based on their function and amino acid sequence similarity [1,2,3,4]
We demonstrated from our laboratory that recombinant human BMP-7 (rhBMP-7) is able to inhibit the atherosclerosis associated inflammation at both acute (Day-14) and mid-stage (Day-28) time points of atherosclerosis by promoting presence of differentiation macrophages along with lymphocytes in M2 atherosclerotic plaques showed enhanced monocyte into the anti-inflammatory phenotype via reducing phosphorylated inflammatory and release of pro-inflammatory molecules
Rocher et al demonstrated that Bone morphogenetic protein-7 is (BMP-7) administration along with apoptotic conditional medium to monocytes resulted in an increased expression of anti-inflammatory cytokines (IL-1ra, IL-10 and arginase-1) and inhibited expression of pro-inflammatory cytokines which promoted paracrine effects on monocytes and macrophages yielding increased M2 macrophage polarization [70]
Summary
In 1970, a physician named Marshall Urist coined the term bone morphogenetic protein (BMP). BMP-2B, BMP2B1, ZYME, OFC11, MCOPS6 major end organs (brain, heart, pancreas, liver, lung, kidney), exocrine gland (prostate), organ protector (skeletal muscle), lymphoid organs (bone marrow, spleen and thymus), spinal cord. OP-1 major end organs (brain, heart, pancreas, liver, lung, kidney), exocrine gland (prostate) organ protector (skeletal muscle), lymphoid organs (bone marrow, spleen and thymus), spinal cord. MGC126783 major end organs (brain, heart, kidney, lung, liver, pancreas), exocrine gland (prostate), organ protector (skeletal muscle), lymphoid organs (spleen, thymus, bone marrow) spinal cord. The focus of this review article was to provide an overall structure of BMP-7, mechanistic pathways and its potential therapeutic significance in CVD
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