Potential of RAS Inhibition to Improve Metabolic Bone Disorders

Abstract

Metabolic bone disorder is usually caused by abnormalities of minerals and hormones metabolism. Recently, it has been proved by several studies that the renin-angiotensin system (RAS) in local bone tissue is directly involved in bone metabolism. Activation of skeletal RAS plays an important role in bone metabolic disorders. Based on in vitro, in vivo, and clinical studies, this review explains the roles of RAS in bone metabolism and also covers the potential approaches and beneficial effects of RAS inhibition on bone health. Differential strategies for inhibiting RAS can be employed to maintain bone health, which are attributed primarily to the reduced level of angiotensin II (AngII) and suppressed stimulation of the AngII signaling pathway. The use of renin inhibitors, angiotensin-converting enzyme inhibitors, and AngII receptor blockers either individually or in combination with each other could have promising results in fighting bone metabolic disorders associated with other cardiovascular diseases as well as independent bone injuries.

Differential Gene Expression Pattern in Osteoclast Precursor Cells of Indian Postmenopausal Women with and Without Osteoporosis: A Microarray Based Study

“…It is known that CSF1 through its receptor c-fms induces proliferation and survival of osteoclasts, whereas ACP5 is a wellknown osteoclast specific marker [28]. Our results of DEGs, TFs, PPIs, gene ontology and previous findings (29)(30)(31)(32)(33)(34) suggest that hematopoietic cells in presence of transcription factor PU.1 form Myeloid/ Monocyte lineage cells like osteoclast precursors [29,30]. CSF1 on binding with its receptor c-fms on osteoclast precursor provides signals for osteoclast proliferation which are manifested through RAS and PI3K dependent mechanisms [31,32].…”

“…CSF1 on binding with its receptor c-fms on osteoclast precursor provides signals for osteoclast proliferation which are manifested through RAS and PI3K dependent mechanisms [31,32]. RAS a small G-protein promotes activation of RAS/PI3K and Raf/MEK/ERK pathway [33]. RAS/PI3K signaling pathway triggers downstream cascade reactions leading to osteoclast survival (Figure4).…”

Tissue Renin–Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease

“…Tissue RAS is also present in bones and involved in bone remodeling (81). In an eight-week interventional study, ARBs improved bone mass and strength in osteoporotic rat femurs (82).…”

Probiotics and Physical Strength

“…Therefore, any alteration in biological mechanism which increases osteoclasts effect or decreases osteoblasts action may results in bone disorder due to change in normal physiology (Gebru et al, 2013). are common pathological condition where the quantity of bone mineral reduction may be due to genetic components characterized by reduced bone mass and increased risk of fractures.…”