scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies 2.0

2020 ◽  
Vol 21 (21) ◽  
pp. 8005
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Trabecular Microarchitecture ◽  
Anabolic Agent ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis. Teriparatide, an anabolic agent, stimulates bone formation and corrects the characteristic changes in the trabecular microarchitecture. However, these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the ten articles published in our Special Issue “Osteoporosis: From Molecular Mechanisms to Therapies 2.0”, a continuation of our 2019 Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies" (https://www.mdpi.com/journal/ijms/special_issues/osteoporosis_ijms). These Special Issues detail important global scientific findings that contribute to our current understanding of osteoporosis.

scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies 3.0

2021 ◽  
Vol 22 (23) ◽  
pp. 12725
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Trabecular Microarchitecture ◽  
Anabolic Agent ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder that occurs as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis. Teriparatide, an anabolic agent, stimulates bone formation and corrects the characteristic changes in the trabecular microarchitecture. However, these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the six articles published in our Special Issue “Osteoporosis: From Molecular Mechanisms to Therapies 3.0”, a continuation of our 2020 Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies". These Special Issues detail important global scientific findings that contribute to our current understanding of osteoporosis.

scholarly journals Osteoporosis: From Molecular Mechanisms to Therapies

2020 ◽  
Vol 21 (3) ◽  
pp. 714 ◽  
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Special Issue ◽  
Anabolic Agents ◽  
Trabecular Microarchitecture ◽  
Stimulate Bone Formation ◽  
Skeletal Disorder

Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis, while anabolic agents such as teriparatide stimulate bone formation and correct the characteristic changes in the trabecular microarchitecture. However, all of these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the fifteen articles published in the Special Issue, Osteoporosis: From Molecular Mechanisms to Therapies 2019, as part of the global picture of the current understanding of osteoporosis.

scholarly journals Overview on the Side Effects of Doxorubicin

2020 ◽  
Author(s):  
Chittipolu Ajaykumar
Keyword(s):  
Side Effects ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Cytotoxic Effect ◽  
Molecular Mechanisms ◽  
Current Understanding ◽  
Preventive Strategies ◽  
Normal Cells ◽  
Dna Strand

Doxorubicin is an anthracycline antibiotic extracted from the bacterium Streptomyces peucetius. Its cytotoxic effect produced by intercalating with DNA causing breakdown of DNA strand which causes cancer cell apoptosis. Despite being an effective anticancer agent it causes several crucial side effects like carditoxicity, neuropathy, hepatotoxicity, nephrotoxicity, alopecia, typhlitis, myelosuppression, neutropenia, anaemia, thrombocytopenia, nausea, and diarrhoea were caused mainly due to the inability to distinguish between cancer cells and normal cells. This chapter mainly focuses on doxorubicin’s side effects, current understanding of the molecular mechanisms, and management and preventive strategies of doxorubicin’s cardiotoxicity during the treatment of various type of cancer.

scholarly journals SCREENING FOR VIETNAMESE PLANT EXTRACTS WITH POTENTIAL BENEFIT FOR ANTI OSTEOCLASTOGENESISH

2021 ◽  
Vol 59 (4) ◽  
pp. 507
Author(s):  
Hai Dang Nguyen ◽  
Thanh Huong Le ◽  
Thu Trang Duong
Keyword(s):  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Plant Extracts ◽  
Potential Benefit ◽  
Mouse Macrophage ◽  
Potential Source ◽  
Inhibitory Activities ◽  
First Time

Bone's homeostasis is only achieved when there is a balance between bone formation and bone resorption. A metabolic disorder of bone-resorbing osteoclasts can lead to osteoporosis. Long-term use of anti-osteoporosis drugs can lead to undesirable side effects so traditional herbal can be a potential source of alternative medicine. In the present study, forty one Vietnamese plants (seventy methanol extracts) were screened for osteoclastogenesis inhibitory activities on RAW264.7 mouse macrophage cells. For the first time, 29 extracts from 24 species showed potential as effective inhibitors of osteoclastogenesis.

scholarly journals Research of Pathogenesis and Novel Therapeutics in Arthritis

2019 ◽  
Vol 20 (7) ◽  
pp. 1646 ◽  
Author(s):  
Chih-Hsin Tang
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Side Effects ◽  
Inflammatory Arthritis ◽  
Current Understanding ◽  
Special Issue ◽  
Novel Therapeutics ◽  
High Prevalence ◽  
Exact Etiology ◽  
Inflammatory Drugs

Arthritis has a high prevalence globally and includes over 100 types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis, but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for these patients. In this editorial, the twenty articles published in the Special Issue Research of Pathogenesis and Novel Therapeutics in Arthritis 2019 are summarized and discussed as part of the global picture of the current understanding of arthritis.

scholarly journals Transcriptomics‐based analysis of the mechanism by which Wang-Bi capsule alleviates joint destruction in rats with collagen‐induced arthritis

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Haiyang Shu ◽  
Hanxiao Zhao ◽  
Yingjie Shi ◽  
Cheng Lu ◽  
Li Li ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Joint Destruction ◽  
Micro Ct ◽  
Collagen Induced Arthritis ◽  
Cartilage Development ◽  
And Cartilage

Abstract Background Rheumatoid arthritis (RA) is a chronic autoimmune disease accompanied with joint destruction that often leads to disability. Wang-Bi capsule (WB), a traditional Chinese medicine-based herbs formula, has exhibited inhibition effect on joint destruction of collagen-induced arthritis (CIA) animal model in our previous study. But its molecular mechanisms are still obscure. Methods CIA rats were treated intragastrical with WB for eight weeks, and the effect of joints protection were evaluated by hematoxylin and eosin (H&E) staining, safranin O fast green staining, tartrate-resistant acid phosphatase (TRAP) staining and micro‑CT scanning analysis. The transcriptomic of tarsal joints were used to investigate how WB alleviated joint destruction. Results The histological examination of ankle joints showed WB alleviated both cartilage damage and bone destruction of CIA rats. This protective effect on joints were further evidenced by micro-CT analysis. The transcriptomic analysis showed that WB prominently changed 12 KEGG signaling pathways (“calcium signaling pathway”, “cAMP signaling pathway”, “cell adhesion molecules”, “chemokine signaling pathway”, “complement and coagulation cascades”, “MAPK signaling pathway”, “NF-kappa B signaling pathway”, “osteoclast differentiation”, “PI3K-Akt signaling pathway”, “focal adhesion”, “Gap junction” and “Rap1 signaling pathway”) associated with bone or cartilage. Several genes (including Il6, Tnfsf11, Ffar2, Plg, Tnfrsf11b, Fgf4, Fpr1, Siglec1, Vegfd, Cldn1, Cxcl13, Chad, Arrb2, Fgf9, Egfr) regulating bone resorption, bone formation and cartilage development were identified by further analysis. Meanwhile, these differentially expressed genes were validated by real-time quantitative PCR. Conclusions Overall, the protective effect of WB treatment on joint were confirmed in CIA rats, and its basic molecular mechanisms may be associated with regulating some genes (including Il6, Tnfsf11, Ffar2 and Plg etc.) involved in bone resorption, bone formation and cartilage development.

scholarly journals Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

2020 ◽  
Vol 47 (4) ◽  
pp. 75-80
Author(s):  
I. Yankova ◽  
A. Shinkov ◽  
R. Kovatcheva
Keyword(s):  
Bone Resorption ◽  
Primary Hyperparathyroidism ◽  
Bone Formation ◽  
Bone Metabolism ◽  
Cortical Bone ◽  
Mineral Density ◽  
Trabecular Microarchitecture ◽  
Duration Of Action ◽  
Increased Risk ◽  
Stimulation Of

AbstractParathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.

scholarly journals Effect of low-dose of recombinant human growth hormone on bone metabolism in elderly women with osteoporosis

2002 ◽  
pp. 339-348 ◽  
Author(s):  
T Sugimoto ◽  
H Kaji ◽  
D Nakaoka ◽  
M Yamauchi ◽  
S Yano ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Lumbar Spine ◽  
Side Effects ◽  
Bone Resorption ◽  
Bone Formation ◽  
Low Dose ◽  
Elderly Women ◽  
Serum Concentrations ◽  
Gh Treatment ◽  
Igf I

BACKGROUND: There has been increasing evidence that the growth hormone (GH)-IGF-I axis plays an important part in the maintenance of bone mass. However, controversy still exists as to the effect of GH treatment on bone mineral density (BMD) in elderly patients with osteoporosis. OBJECTIVE: To investigate the effect of low-dose GH treatment on markers of body composition and bone turnover, serum concentrations of IGF-I and IGF-binding proteins (IGFBPs), and BMD at the radius and lumbar spine in eight elderly Japanese women with osteoporosis. METHODS: Participants were treated with GH as a single daily subcutaneous injection (0.125 IU/kg per week; 0.00595 mg/kg per day) for 48 weeks. RESULTS: Markers of bone formation and bone resorption were both increased up to 24 weeks of GH treatment. The bone formation markers remained increased during GH treatment, whereas the bone resorption markers returned to baseline values after 24 weeks of GH treatment. GH treatment caused a rapid (within 2 weeks) and sustained increase in serum IGF-I concentration. As for IGFBPs, serum concentrations of IGFBPs-2, -3 and -4 did not change significantly during GH treatment. In contrast, GH treatment caused a gradual increase in serum IGFBP-5 concentration, with a significant increase seen 48 weeks after the start of GH treatment. Radial BMD seemed to be increased during the late period of GH treatment, although the change was not significant. Lumbar BMD did not change during GH treatment. GH treatment caused a significant increase in hand grip strength. None of the GH-treated participants had new fractures and side effects such as edema and joint pain. Radial BMD was significantly increased after discontinuation of GH treatment for another 48 weeks and a similar tendency was observed at the lumbar spine (7.1+/-2.3% above pretreatment values for the radius and 3.6+/-2.0% for the lumbar spine). CONCLUSIONS: Low-dose GH treatment attenuated the decrease in muscle strength and bone mass in elderly women without side effects, although changes in nutrition and exercise might affect BMD. The present findings provide useful information regarding the use of low-dose GH treatment in elderly women with osteoporosis.

scholarly journals The bone remodelling cycle

2018 ◽  
Vol 55 (3) ◽  
pp. 308-327 ◽  
Author(s):  
JS Kenkre ◽  
JHD Bassett
Keyword(s):  
Bone Resorption ◽  
Bone Formation ◽  
Bone Disease ◽  
Molecular Mechanisms ◽  
Bone Remodelling ◽  
Nuclear Factor Κb ◽  
Pharmacological Interventions ◽  
Osteoblastic Bone Formation ◽  
Metabolic Bone ◽  
Tightly Coupled

The bone remodelling cycle replaces old and damaged bone and is a highly regulated, lifelong process essential for preserving bone integrity and maintaining mineral homeostasis. During the bone remodelling cycle, osteoclastic resorption is tightly coupled to osteoblastic bone formation. The remodelling cycle occurs within the basic multicellular unit and comprises five co-ordinated steps; activation, resorption, reversal, formation and termination. These steps occur simultaneously but asynchronously at multiple different locations within the skeleton. Study of rare human bone disease and animal models have helped to elucidate the cellular and molecular mechanisms that regulate the bone remodelling cycle. The key signalling pathways controlling osteoclastic bone resorption and osteoblastic bone formation are receptor activator of nuclear factor-κB (RANK)/RANK ligand/osteoprotegerin and canonical Wnt signalling. Cytokines, growth factors and prostaglandins act as paracrine regulators of the cycle, whereas endocrine regulators include parathyroid hormone, vitamin D, calcitonin, growth hormone, glucocorticoids, sex hormones, and thyroid hormone. Disruption of the bone remodelling cycle and any resulting imbalance between bone resorption and formation leads to metabolic bone disease, most commonly osteoporosis. The advances in understanding the cellular and molecular mechanisms underlying bone remodelling have also provided targets for pharmacological interventions which include antiresorptive and anabolic therapies. This review will describe the remodelling process and its regulation, discuss osteoporosis and summarize the commonest pharmacological interventions used in its management.

scholarly journals The Molecular Mechanism of Vitamin E as a Bone-Protecting Agent: A Review on Current Evidence

2019 ◽  
Vol 20 (6) ◽  
pp. 1453 ◽  
Author(s):  
Sok Wong ◽  
Nur-Vaizura Mohamad ◽  
Nurul Ibrahim ◽  
Kok-Yong Chin ◽  
Ahmad Shuid ◽  
...  
Keyword(s):  
Vitamin E ◽  
Bone Resorption ◽  
Bone Formation ◽  
Molecular Mechanisms ◽  
Nuclear Factor Kappa B ◽  
Bone Remodelling ◽  
Current Evidence ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

Bone remodelling is a tightly-coordinated and lifelong process of replacing old damaged bone with newly-synthesized healthy bone. In the bone remodelling cycle, bone resorption is coupled with bone formation to maintain the bone volume and microarchitecture. This process is a result of communication between bone cells (osteoclasts, osteoblasts, and osteocytes) with paracrine and endocrine regulators, such as cytokines, reactive oxygen species, growth factors, and hormones. The essential signalling pathways responsible for osteoclastic bone resorption and osteoblastic bone formation include the receptor activator of nuclear factor kappa-B (RANK)/receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG), Wnt/β-catenin, and oxidative stress signalling. The imbalance between bone formation and degradation, in favour of resorption, leads to the occurrence of osteoporosis. Intriguingly, vitamin E has been extensively reported for its anti-osteoporotic properties using various male and female animal models. Thus, understanding the underlying cellular and molecular mechanisms contributing to the skeletal action of vitamin E is vital to promote its use as a potential bone-protecting agent. This review aims to summarize the current evidence elucidating the molecular actions of vitamin E in regulating the bone remodelling cycle.

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