Novel therapies for osteoporosis

Makras, Polyzois; Delaroudis, S.; Anastasilakis, Athanasios D.

doi:10.1016/j.metabol.2015.07.011

Cited by 66 publications

(44 citation statements)

References 128 publications

(142 reference statements)

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“…The identification and validation of novel biomarkers for osteoporosis is a high priority not only for identifying patients at high risk for fracture and monitoring the efficacy of anti-resorptive therapies, but also for defining novel therapeutic strategies (Makras et al, 2015). Despite great advances in the understanding of mechanisms in bone metabolism over the past few years, major limitations still exist in managing osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

“…In osteoporosis, the balance between osteoclast and osteoblast activities is disrupted. The dysregulation of bone resorbing osteoclasts significantly contributes to aging and drug-induced osteoporosis (Makras et al, 2015). MicroRNAs (miRNAs) are a class of endogenous, non-coding, singlestranded RNAs 19-24 nucleotides in length, which block translation or initiate transcript degradation via binding to the 3'-untranslated region (3'-UTR) of target mRNAs (Zamore and Haley, 2005).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting

Zhang

Geng

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The differentiation deficiencies of osteoclast precursors (pre-OCs) may contribute to osteoporosis. Research on osteoporosis has recently focused on microRNAs (miRNAs) that play crucial roles in pre-OC differentiation. In the current study, we aimed to analyze the expression and function of the glucocorticoid (GC)-associated miRNA-338-3p (miR-338-3p) in osteoclast formation. We found that dexamethasone induced osteoclast differentiation and inhibited miR-338-3p expression. Overexpression of an miR-338-3p mimic in osteoclast precursor cells attenuated GC-induced osteoclast formation and bone resorption, whereas inhibition of miR-338-3p reversed these effects. The expression of the nuclear factor κB ligand RANKL, a 2 X.H. Zhang et al. Genetics and Molecular Research 15 (3): gmr.15037674 potential target gene of miR-338-3p, was inversely correlated with miR-338-3p expression in pre-OCs. Furthermore, we demonstrated that RANKL was directly regulated by miR-338-3p and re-introduction of RANKL reversed the inhibitory effects of miR-338-3p on osteoclast formation and bone resorption. Taken together, these findings demonstrate that miR-338-3p may play a significant role in GCinduced osteoclast differentiation and function by targeting RANKL in osteoclasts.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting

Zhang

Geng

et al. 2016

Genet. Mol. Res.

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“…A single dose administered to ovariectomized rats led to a maximum increase of 14% in vertebral BMD compared to a temporary 5% increase with daily PTH administration [53]. Various drugs have also been chemically modified or conjugated with the phosphate-carbon-phosphate (P-C-P) moiety that characterizes bisphosphonates to increase affinity for the bone surface.…”

Section: Osteoporosis Treatmentsmentioning

confidence: 99%

Advances in Controlled Drug Delivery for Treatment of Osteoporosis

Asafo-Adjei

Chen

Najarzadeh

et al. 2016

Curr Osteoporos Rep

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Osteoporosis, which is characterized by resorption of bone exceeding formation, remains a significant human health concern, and the impact of this condition will only increase with the “greying” of the worldwide population. This review focuses on current and emerging approaches for delivering therapeutic agents to restore bone remodeling homeostasis. Well-known antiresorptive and anabolic agents such as estrogen, estrogen analogs, bisphosphonates, calcitonin, and parathyroid hormone, along with newer modulators and antibodies, are primarily administered orally, intravenously, or subcutaneously. Although these treatments can be effective, continuing problems include patient non-compliance and adverse systemic or remote-site effects. Controlled drug delivery via polymeric, targeted, and active release systems extends drug half-life by shielding against premature degradation and improves bioavailability, while also providing prolonged, sustained, or intermittent release at therapeutic doses to more effectively treat osteoporosis and associated fracture risk.

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“…Odanacatib, an inhibitor of cathepsin K, exhibits similar bone protection effects, and approval can be expected soon. Other agents, such as a PTH-related peptide (PTHrp) analog and a Src tyrosine kinase inhibitor, are at the stage of clinical or preclinical evaluations (Makras et al, 2015;Suresh and Abrahamsen, 2015).…”

Section: Op (Osteoporosis)mentioning

confidence: 99%

Osteoimmunology: memorandum for rheumatologists

Huang

Zhang

2016

Sci. China Life Sci.

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Rapid progress has been made in exploring the connections between the skeletal system and the immune system over the past decade. Bone tissue forms developmental niches for hematopoietic stem cells, and activated immune cells are involved in bone metabolism regulation and are potent mediators of osteoporosis and bone erosion under pathological conditions. The interdisciplinary field of osteoimmunology has emerged to pool the knowledge of the interdependence of these two systems, including the shared ligands and receptors, their crosstalk and interaction, and common intracellular signaling pathways with bidirectional influence. The receptor activator of nuclear factor-kappa B (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) triad is the key vinculum, with multifaceted potency, being not only essential for osteoclastogenesis but also critical for lymph node organogenesis and lymphopoiesis as well as for immune regulation. In this review, we summarize the progress in this area, focusing on those aspects of interest concerning rheumatic diseases. osteoimmunology, bone remodeling, osteoclastogenesis, immune cells, RANKLCitation:

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Novel therapies for osteoporosis

Cited by 66 publications

References 128 publications

MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting

MicroRNA-338-3p inhibits glucocorticoid-induced osteoclast formation through RANKL targeting

Advances in Controlled Drug Delivery for Treatment of Osteoporosis

Osteoimmunology: memorandum for rheumatologists

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