Collagen and non-collagenous proteins molecular crosstalk in the pathophysiology of osteoporosis. (October 2019)
- Record Type:
- Journal Article
- Title:
- Collagen and non-collagenous proteins molecular crosstalk in the pathophysiology of osteoporosis. (October 2019)
- Main Title:
- Collagen and non-collagenous proteins molecular crosstalk in the pathophysiology of osteoporosis
- Authors:
- Licini, Caterina
Vitale-Brovarone, Chiara
Mattioli-Belmonte, Monica - Abstract:
- Graphical abstract: Representative drawing of the interaction between an osteoclast (OC; in violet) and osteoblasts (OBs; in red) and ECM. Collagen and NCPs networking. Highlights: Normal or pathological connections between Collagen and NCPs in bone matrix formation and resorption are far from being elucidated. Anomalies in their amount and structure can cause malformations and defects, such as osteoporosis (OP). Collagen and NCPs crosstalk and possible involvement in OP onset and maintenance is focused. These elements can be useful for the design/development of innovative strategies in bone remodelling. Abstract: Collagenous and non-collagenous proteins (NCPs) in the extracellular matrix, as well as the coupling mechanisms between osteoclasts and osteoblasts, work together to ensure normal bone metabolism. Each protein plays one or more critical roles in bone metabolism, sometimes even contradictory, thus affecting the final mechanical, physical and chemical properties of bone tissue. Anomalies in the amount and structure of one or more of these proteins can cause abnormalities in bone formation and resorption, which consequently leads to malformations and defects, such as osteoporosis (OP). The connections between key proteins involved in matrix formation and resorption are far from being elucidated. In this review, we resume knowledge on the crosstalk between collagen type I and selected NCPs (Transforming Growth Factor-β, Insulin-like Growth Factor-1, Decorin,Graphical abstract: Representative drawing of the interaction between an osteoclast (OC; in violet) and osteoblasts (OBs; in red) and ECM. Collagen and NCPs networking. Highlights: Normal or pathological connections between Collagen and NCPs in bone matrix formation and resorption are far from being elucidated. Anomalies in their amount and structure can cause malformations and defects, such as osteoporosis (OP). Collagen and NCPs crosstalk and possible involvement in OP onset and maintenance is focused. These elements can be useful for the design/development of innovative strategies in bone remodelling. Abstract: Collagenous and non-collagenous proteins (NCPs) in the extracellular matrix, as well as the coupling mechanisms between osteoclasts and osteoblasts, work together to ensure normal bone metabolism. Each protein plays one or more critical roles in bone metabolism, sometimes even contradictory, thus affecting the final mechanical, physical and chemical properties of bone tissue. Anomalies in the amount and structure of one or more of these proteins can cause abnormalities in bone formation and resorption, which consequently leads to malformations and defects, such as osteoporosis (OP). The connections between key proteins involved in matrix formation and resorption are far from being elucidated. In this review, we resume knowledge on the crosstalk between collagen type I and selected NCPs (Transforming Growth Factor-β, Insulin-like Growth Factor-1, Decorin, Osteonectin, Osteopontin, Bone Sialoprotein and Osteocalcin) of bone matrix, focusing on their possible involvement and role in OP. The different elements of this network can be pharmacologically targeted or used for the design/development of innovative regenerative strategies to modulate a feedback loop in bone remodelling. … (more)
- Is Part Of:
- Cytokine & growth factor reviews. Volume 49(2019)
- Journal:
- Cytokine & growth factor reviews
- Issue:
- Volume 49(2019)
- Issue Display:
- Volume 49, Issue 2019 (2019)
- Year:
- 2019
- Volume:
- 49
- Issue:
- 2019
- Issue Sort Value:
- 2019-0049-2019-0000
- Page Start:
- 59
- Page End:
- 69
- Publication Date:
- 2019-10
- Subjects:
- 1, 25(OH)2D3 1, 25-dihydroxy vitamin D3 -- AGEs advanced glycation end products -- ALP alkaline phosphatase -- BGLAP bone gamma-carboxyglutamic acid-containing protein -- BMD bone mineral density -- BMSCs bone mesenchymal stem cells -- CatK cathepsin K -- COL1A1 collagen alpha-1(I) chain -- CTx C-terminal telopeptide -- DCN decorin -- DPD deoxypyridinoline -- DPL deoxypyrrololine -- EC EF-hand Ca2+- binding -- ECM extracellular matrix -- FS follistatin -- GAGs glycosaminoglycans -- GLA γ-carboxyglutamate -- HA hydroxyapatite -- HRT hormone replacement therapy -- Hyl hydroxylysine -- IGF-1 insulin-like growth factor-1 -- IGFBPs insulin-like growth factor binding proteins -- LAP latency-associated protein -- LRRs leucine-rich repeats -- LTBP latent TGF-β Binding Protein -- Lys lysine -- M-CSF macrophage colony-stimulating factor -- MMPs matrix metalloproteases -- NCPs non-collagenous Proteins -- NTx N-terminal Telopeptide -- OBs osteoblasts -- OCN osteocalcin -- OCs osteoclasts -- OCYs osteocytes -- ON osteonectin -- OP osteoporosis -- OPG osteoprotegerin -- OPN osteopontin -- OVX ovariectomized -- PDGF platelet-derived growth factor -- PTH parathyroid Hormone -- PYD pyridinium -- PYL pyrrole -- RAGEs receptors for advanced glycation end products -- RANKL receptor activator of nuclear factor Kappa-Β ligand -- RGD Arg-Gly-Asp sequence -- RUNX2 runt-related transcription factor 2 -- SIBLING small integrin binding ligand N-glycosylated -- SLRP small leucine-rich proteoglycan -- SPARC secreted protein acidic and rich in cysteine -- TβRI TGF-β receptor type I -- TβRII TGF-β receptor type II -- TGF-β transforming growth factor-β -- WT wild-type
Osteoporosis -- Type I collagen -- NCPs -- Transforming growth factor-β -- Insulin-like growth Factor-1 -- Osteopontin
Cytokines -- Periodicals
571.84 - Journal URLs:
- http://www.sciencedirect.com/science/journal/13596101 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.cytogfr.2019.09.001 ↗
- Languages:
- English
- ISSNs:
- 1359-6101
- Deposit Type:
- Legaldeposit
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- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
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