|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | TGF-β and BMP signaling in osteoblast,skeletal development,and bone formation,homeostasis and disease显示文摘Transforming growth factor-beta(TGF-β) and bone morphogenic protein(BMP) signaling has fundamental roles in both embryonic skeletal development and postnatal bone homeostasis.TGF-βs and BMPs,acting on a tetrameric receptor complex,transduce signals to both the canonical Smad-dependent signaling pathway(that is,TGF-β/BMP ligands,receptors,and Smads) and the non-canonical-Smad-independent signaling pathway(that is,p38 mitogen-activated protein kinase/p38 MAPK) to regulate mesenchymal stem cell differentiation during skeletal development,bone formation and bone homeostasis.Both the Smad and p38 MAPK signaling pathways converge at transcription factors,for example,Runx2 to promote osteoblast differentiation and chondrocyte differentiation from mesenchymal precursor cells.TGF-β and BMP signaling is controlled by multiple factors,including the ubiquitin–proteasome system,epigenetic factors,and micro RNA.Dysregulated TGF-β and BMP signaling result in a number of bone disorders in humans.Knockout or mutation of TGF-β and BMP signaling-related genes in mice leads to bone abnormalities of varying severity,which enable a better understanding of TGF-β/BMP signaling in bone and the signaling networks underlying osteoblast differentiation and bone formation.There is also crosstalk between TGF-β/BMP signaling and several critical cytokines' signaling pathways(for example,Wnt,Hedgehog,Notch,PTHr P,and FGF) to coordinate osteogenesis,skeletal development,and bone homeostasis.This review summarizes the recent advances in our understanding of TGF-β/BMP signaling in osteoblast differentiation,chondrocyte differentiation,skeletal development,cartilage formation,bone formation,bone homeostasis,and related human bone diseases caused by the disruption of TGF-β/BMP signaling. | Mengrui Wu Guiqian Chen Yi-Ping Li | 2016 | Bone Research2016，4，1： | 123 |
| 2 | Osteoarthritis:toward a comprehensive understanding of pathological mechanism显示文摘Osteoarthritis(OA) is the most common degenerative joint disease and a major cause of pain and disability in adult individuals. The etiology of OA includes joint injury, obesity, aging, and heredity. However, the detailed molecular mechanisms of OA initiation and progression remain poorly understood and, currently,there are no interventions available to restore degraded cartilage or decelerate disease progression. The diathrodial joint is a complicated organ and its function is to bear weight, perform physical activity and exhibit a joint-specific range of motion during movement. During OA development, the entire joint organ is affected, including articular cartilage, subchondral bone, synovial tissue and meniscus. A full understanding of the pathological mechanism of OA development relies on the discovery of the interplaying mechanisms among different OA symptoms, including articular cartilage degradation, osteophyte formation, subchondral sclerosis and synovial hyperplasia, and the signaling pathway(s) controlling these pathological processes. | Di Chen Jie Shen Weiwei Zhao Tingyu Wang Lin Han John L Hamilton Hee-Jeong Im | 2017 | Bone Research2017，5，1： | 121 |
| 3 | Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies显示文摘Rheumatoid arthritis(RA) is a chronic systemic autoimmune disease that primarily affects the lining of the synovial joints and is associated with progressive disability, premature death, and socioeconomic burdens. A better understanding of how the pathological mechanisms drive the deterioration of RA progress in individuals is urgently required in order to develop therapies that will effectively treat patients at each stage of the disease progress. Here we dissect the etiology and pathology at specific stages:(i) triggering,(ii) maturation,(iii) targeting, and(iv) fulminant stage, concomitant with hyperplastic synovium, cartilage damage, bone erosion, and systemic consequences. Modern pharmacologic therapies(including conventional, biological, and novel potential small molecule disease-modifying anti-rheumatic drugs) remain the mainstay of RA treatment and there has been significant progress toward achieving disease remission without joint deformity. Despite this, a significant proportion of RA patients do not effectively respond to the current therapies and thus new drugs are urgently required. This review discusses recent advances of our understanding of RA pathogenesis, disease modifying drugs, and provides perspectives on next generation therapeutics for RA. | Qiang Guo Yuxiang Wang Dan Xu Johannes Nossent Nathan J.Pavlos Jiake Xu | 2018 | Bone Research2018，6，2： | 71 |
| 4 | TGF-β/BMP signaling and other molecular events: regulation of osteoblastogenesis and bone formation显示文摘Transforming growth factor-beta(TGF-β)/bone morphogenetic protein(BMP) plays a fundamental role in the regulation of bone organogenesis through the activation of receptor serine/threonine kinases. Perturbations of TGF-β/BMP activity are almost invariably linked to a wide variety of clinical outcomes, i.e., skeletal, extra skeletal anomalies, autoimmune, cancer, and cardiovascular diseases. Phosphorylation of TGF-β(I/II) or BMP receptors activates intracellular downstream Smads, the transducer of TGF-β/BMP signals. This signaling is modulated by various factors and pathways, including transcription factor Runx2. The signaling network in skeletal development and bone formation is overwhelmingly complex and highly time and space specific.Additive, positive, negative, or synergistic effects are observed when TGF-β/BMP interacts with the pathways of MAPK, Wnt, Hedgehog(Hh), Notch, Akt/m TOR, and mi RNA to regulate the effects of BMP-induced signaling in bone dynamics. Accumulating evidence indicates that Runx2 is the key integrator, whereas Hh is a possible modulator, mi RNAs are regulators, and b-catenin is a mediator/regulator within the extensive intracellular network. This review focuses on the activation of BMP signaling and interaction with other regulatory components and pathways highlighting the molecular mechanisms regarding TGF-β/BMP function and regulation that could allow understanding the complexity of bone tissue dynamics. | Md Shaifur Rahman Naznin Akhtar Hossen Mohammad Jamil Rajat Suvra Banik Sikder M Asaduzzaman | 2015 | Bone Research2015，3，1： | 53 |
| 5 | Paracrine and endocrine actions of bone——the functions of secretory proteins from osteoblasts, osteocytes, and osteoclasts显示文摘The skeleton is a dynamic organ that is constantly remodeled. Proteins secreted from bone cells, namely osteoblasts, osteocytes,and osteoclasts exert regulation on osteoblastogenesis, osteclastogenesis, and angiogenesis in a paracrine manner. Osteoblasts secrete a range of different molecules including RANKL/OPG, M-CSF, SEMA3A, WNT5A, and WNT16 that regulate osteoclastogenesis. Osteoblasts also produce VEGFA that stimulates osteoblastogenesis and angiogenesis. Osteocytes produce sclerostin(SOST) that inhibits osteoblast differentiation and promotes osteoclast differentiation. Osteoclasts secrete factors including BMP6, CTHRC1, EFNB2, S1P, WNT10B, SEMA4D, and CT-1 that act on osteoblasts and osteocytes, and thereby influencea A osteogenesis. Osteoclast precursors produce the angiogenic factor PDGF-BB to promote the formation of Type H vessels, which then stimulate osteoblastogenesis. Besides, the evidences over the past decades show that at least three hormones or 'osteokines'from bone cells have endocrine functions. FGF23 is produced by osteoblasts and osteocytes and can regulate phosphate metabolism. Osteocalcin(OCN) secreted by osteoblasts regulates systemic glucose and energy metabolism, reproduction, and cognition. Lipocalin-2(LCN2) is secreted by osteoblasts and can influence energy metabolism by suppressing appetite in the brain.We review the recent progresses in the paracrine and endocrine functions of the secretory proteins of osteoblasts, osteocytes, and osteoclasts, revealing connections of the skeleton with other tissues and providing added insights into the pathogenesis of degenerative diseases affecting multiple organs and the drug discovery process. | Yujiao Han Xiuling You Wenhui Xing Zhong Zhang Weiguo Zou | 2018 | Bone Research2018，6，2： | 52 |
| 6 | Injectable hydrogels for cartilage and bone tissue engineering显示文摘Tissue engineering has become a promising strategy for repairing damaged cartilage and bone tissue. Among the scaffolds for tissue-engineering applications, injectable hydrogels have demonstrated great potential for use as three-dimensional cell culture scaffolds in cartilage and bone tissue engineering, owing to their high water content, similarity to the natural extracellular matrix(ECM), porous framework for cell transplantation and proliferation, minimal invasive properties, and ability to match irregular defects. In this review, we describe the selection of appropriate biomaterials and fabrication methods to prepare novel injectable hydrogels for cartilage and bone tissue engineering. In addition, the biology of cartilage and the bony ECM is also summarized. Finally, future perspectives for injectable hydrogels in cartilage and bone tissue engineering are discussed. | Mei Liu Xin Zeng Chao Ma Huan Yi Zeeshan Ali Xianbo Mou Song Li Yan Deng Nongyue He | 2017 | Bone Research2017，5，2： | 54 |
| 7 | Bone Regeneration Based on Tissue Engineering Conceptions – A 21st Century Perspective显示文摘The role of Bone Tissue Engineering in the field of Regenerative Medicine has been the topic of substantial research over the past two decades.Technological advances have improved orthopaedic implants and surgical techniques for bone reconstruction.However,improvements in surgical techniques to reconstruct bone have been limited by the paucity of autologous materials available and donor site morbidity.Recent advances in the development of biomaterials have provided attractive alternatives to bone grafting expanding the surgical options for restoring the form and function of injured bone.Specifically,novel bioactive(second generation)biomaterials have been developed that are characterised by controlled action and reaction to the host tissue environment,whilst exhibiting controlled chemical breakdown and resorption with an ultimate replacement by regenerating tissue.Future generations of biomaterials(third generation)are designed to be not only osteoconductive but also osteoinductive,i.e.to stimulate regeneration of host tissues by combining tissue engineering and in situ tissue regeneration methods with a focus on novel applications.These techniques will lead to novel possibilities for tissue regeneration and repair.At present,tissue engineered constructs that may find future use as bone grafts for complex skeletal defects,whether from post-traumatic,degenerative,neoplastic or congenital/developmental'origin'require osseous reconstruction to ensure structural and functional integrity.Engineering functional bone using combinations of cells,scaffolds and bioactive factors is a promising strategy and a particular feature for future development in the area of hybrid materials which are able to exhibit suitable biomimetic and mechanical properties.This review will discuss the state of the art in this field and what we can expect from future generations of bone regeneration concepts. | Jan Henkel Maria A.Woodruff Devakara R.Epari Roland Steck Vaida Glatt Ian C.Dickinson Peter F.M.Choong Michael A.Schuetz Dietmar W.Hutmacher | 2013 | Bone Research2013，1，3： | 33 |
| 8 | Application of platelet-rich plasma with stem cells in bone and periodontal tissue engineering显示文摘Presently, there is a high paucity of bone grafts in the United States and worldwide. Regenerating bone is of prime concern due to the current demand of bone grafts and the increasing number of diseases causing bone loss. Autogenous bone is the present gold standard of bone regeneration. However, disadvantages like donor site morbidity and its decreased availability limit its use. Even allografts and synthetic grafting materials have their own limitations. As certain specific stem cells can be directed to differentiate into an osteoblastic lineage in the presence of growth factors(GFs), it makes stem cells the ideal agents for bone regeneration.Furthermore, platelet-rich plasma(PRP), which can be easily isolated from whole blood, is often used for bone regeneration, wound healing and bone defect repair. When stem cells are combined with PRP in the presence of GFs, they are able to promote osteogenesis. This review provides in-depth knowledge regarding the use of stem cells and PRP in vitro, in vivo and their application in clinical studies in the future. | Gabriela Fernandes Shuying Yang | 2016 | Bone Research2016，4，4： | 31 |
| 9 | Ankylosing spondylitis: etiology, pathogenesis, and treatments显示文摘Ankylosing spondylitis(AS), a common type of spondyloarthropathy, is a chronic inflammatory autoimmune disease that mainly affects spine joints, causing severe, chronic pain;additionally, in more advanced cases, it can cause spine fusion. Significant progress in its pathophysiology and treatment has been achieved in the last decade. Immune cells and innate cytokines have been suggested to be crucial in the pathogenesis of AS, especially human leukocyte antigen(HLA)?B27 and the interleukin?23/17 axis.However, the pathogenesis of AS remains unclear. The current study reviewed the etiology and pathogenesis of AS, including genome-wide association studies and cytokine pathways. This study also summarized the current pharmaceutical and surgical treatment with a discussion of future potential therapies. | Wei Zhu Xuxia He Kaiyuan Cheng Linjie Zhang Di Chen Xiao Wang Guixing Qiu Xu Cao Xisheng Weng | 2019 | Bone Research2019，7，3： | 30 |
| 10 | Bone–cartilage crosstalk:a conversation for understanding osteoarthritis显示文摘Although cartilage degradation is the characteristic feature of osteoarthritis(OA), it is now recognized that the whole joint is involved in the progression of OA. In particular, the interaction(crosstalk) between cartilage and subchondral bone is thought to be a central feature of this process. The interface between articular cartilage and bone of articulating long bones is a unique zone, which comprises articular cartilage,below which is the calcified cartilage sitting on and intercalated into the subchondral bone plate. Below the subchondral plate is the trabecular bone at the end of the respective long bones. In OA, there are welldescribed progressive destructive changes in the articular cartilage, which parallel characteristic changes in the underlying bone. This review examines the evidence that biochemical and biomechanical signaling between these tissue compartments is important in OA disease progression and asks whether such signaling might provide possibilities for therapeutic intervention to halt or slow disease development. | David M Findlay Julia S Kuliwaba | 2016 | Bone Research2016，4，3： | 27 |
| 11 | Autophagy in bone homeostasis and the onset of osteoporosis显示文摘Autophagy is an evolutionarily conserved intracellular process,in which domestic cellular components are selectively digested for the recycling of nutrients and energy.This process is indispensable for cell homeostasis maintenance and stress responses.Both genetic and functional studies have demonstrated that multiple proteins involved in autophagic activities are critical to the survival,differentiation,and functioning of bone cells,including osteoblasts,osteocytes,and osteoclasts.Dysregulation at the level of autophagic activity consequently disturbs the balance between bone formation and bone resorption and mediates the onset and progression of multiple bone diseases,including osteoporosis.This review aims to introduce the topic of autophagy,summarize the understanding of its relevance in bone physiology,and discuss its role in the onset of osteoporosis and therapeutic potential. | Xing Yin Chenchen Zhou Jingtao Li Renkai Liu Bing Shi Quan Yuan Shujuan Zou | 2019 | Bone Research2019，7，4： | 25 |
| 12 | RANKL signaling in bone marrow mesenchymal stem cells negatively regulates osteoblastic bone formation显示文摘RANKL signaling is essential for osteoclastogenesis. Its role in osteoblastic differentiation and bone formation is unknown. Here we demonstrate that RANK is expressed at an early stage of bone marrow mesenchymal stem cells(BMSCs) during osteogenic differentiation in both mice and human and decreased rapidly. RANKL signaling inhibits osteogenesis by promoting β-catenin degradation and inhibiting its synthesis. In contrast, RANKL signaling has no significant effects on adipogenesis of BMSCs.Interestingly, conditional knockout of rank in BMSCs with Prx1-Cre mice leads to a higher bone mass and increased trabecular bone formation independent of osteoclasts. In addition, rank^(flox/flox): Prx1-Cre mice show resistance to ovariectomy-(OVX) induced bone loss. Thus, our results reveal that RANKL signaling regulates both osteoclasts and osteoblasts by inhibition of osteogenic differentiation of BMSCs and promotion of osteoclastogenesis. | Xiao Chen Xin Zhi Jun Wang Jiacan Su | 2018 | Bone Research2018，6，4： | 24 |
| 13 | Molecular mechanosensors in osteocytes显示文摘Osteocytes, the most abundant and long-lived cells in bone, are the master regulators of bone remodeling. In addition to their functions in endocrine regulation and calcium and phosphate metabolism, osteocytes are the major responsive cells in force adaptation due to mechanical stimulation. Mechanically induced bone formation and adaptation, disuse-induced bone loss and skeletal fragility are mediated by osteocytes, which sense local mechanical cues and respond to these cues in both direct and indirect ways. The mechanotransduction process in osteocytes is a complex but exquisite regulatory process between cells and their environment, between neighboring cells, and between different functional mechanosensors in individual cells. Over the past two decades, great efforts have focused on finding various mechanosensors in osteocytes that transmit extracellular mechanical signals into osteocytes and regulate responsive gene expression. The osteocyte cytoskeleton, dendritic processes, Integrin-based focal adhesions, connexin-based intercellular junctions, primary cilium, ion channels, and extracellular matrix are the major mechanosensors in osteocytes reported so far with evidence from both in vitro and in vitro studies. This review aims to give a systematic introduction to osteocyte mechanobiology, provide details of osteocyte mechanosensors, and discuss the roles of osteocyte mechanosensitive signaling pathways in the regulation of bone homeostasis. | Lei Qin Wen Liu Huiling Cao Guozhi Xiao | 2020 | Bone Research2020，8，2： | 24 |
| 14 | Painful intervertebral disc degeneration and inflammation:from laboratory evidence to clinical interventions显示文摘Low back pain(LBP),as a leading cause of disability,is a common musculoskeletal disorder that results in major social and economic burdens.Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration,a significant contributor to LBP.Inflammatory mediators also play an indispensable role in discogenic LBP.The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies.Here,an overview of the advances in inflammation-related pain in disc degeneration is provided,with a discussion on the role of inflammation in IVD degeneration and pain induction.Puncture models,mechanical models,and spontaneous models as the main animal models to study painful disc degeneration are discussed,and the underlying signaling pathways are summarized.Furthermore,potential drug candidates,either under laboratory investigation or undergoing clinical trials,to suppress discogenic LBP by eliminating inflammation are explored.We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research. | Feng-Juan Lyu Haowen Cui Hehai Pan Kenneth MC Cheung Xu Cao James C.Iatridis Zhaomin Zheng | 2021 | Bone Research2021，9，1： | 24 |
| 15 | Subchondral bone microenvironment in osteoarthritis and pain显示文摘Osteoarthritis comprises several joint disorders characterized by articular cartilage degeneration and persistent pain,causing disability and economic burden.The incidence of osteoarthritis is rapidly increasing worldwide due to aging and obesity trends.Basic and clinical research on osteoarthritis has been carried out for decades,but many questions remain unanswered.The exact role of subchondral bone during the initiation and progression osteoarthritis remains unclear.Accumulating evidence shows that subchondral bone lesions,including bone marrow edema and angiogenesis,develop earlier than cartilage degeneration.Clinical interventions targeting subchondral bone have shown therapeutic potential,while others targeting cartilage have yielded disappointing results.Abnormal subchondral bone remodeling,angiogenesis and sensory nerve innervation contribute directly or indirectly to cartilage destruction and pain.This review is about bone-cartilage crosstalk,the subchondral microenvironment and the critical role of both in osteoarthritis progression.It also provides an update on the pathogenesis of and interventions for osteoarthritis and future research targeting subchondral bone. | Yan Hu Xiao Chen Sicheng Wang Yingying Jing Jiacan Su | 2021 | Bone Research2021，9，3： | 24 |
| 16 | Nanomaterials and bone regeneration显示文摘The worldwide incidence of bone disorders and conditions has been increasing. Bone is a nanomaterials composed of organic(mainly collagen) and inorganic(mainly nano-hydroxyapatite) components, with a hierarchical structure ranging from nanoscale to macroscale. In consideration of the serious limitation in traditional therapies, nanomaterials provide some new strategy in bone regeneration. Nanostructured scaffolds provide a closer structural support approximation to native bone architecture for the cells and regulate cell proliferation, differentiation, and migration, which results in the formation of functional tissues. In this article,we focused on reviewing the classification and design of nanostructured materials and nanocarrier materials for bone regeneration, their cell interaction properties, and their application in bone tissue engineering and regeneration. Furthermore, some new challenges about the future research on the application of nanomaterials for bone regeneration are described in the conclusion and perspectives part. | Tao Gong Jing Xie Jinfeng Liao Tao Zhang Shiyu Lin Yunfeng Lin | 2015 | Bone Research2015，3，3： | 23 |
| 17 | Exercise-induced irisin in bone and systemic irisin administration reveal new regulatory mechanisms of bone metabolism显示文摘Irisin is a polypeptide hormone derived from the proteolytic cleavage of fibronectin-type III domaincontaining 5(FNDC5) protein. Once released to circulation upon exercise or cold exposure, irisin stimulates browning of white adipose tissue(WAT) and uncoupling protein 1(UCP1) expression, leading to an increase in total body energy expenditure by augmented UCP1-mediated thermogenesis. It is currently unknown whether irisin is secreted by bone upon exercise or whether it regulates bone metabolism in vivo. In this study, we found that 2 weeks of voluntary wheel-running exercise induced high levels of FNDC5 messenger RNA as well as FNDC5/irisin protein expression in murine bone tissues. Increased immunoreactivity due to exercise-induced FNDC5/irisin expression was detected in different regions of exercised femoral bones,including growth plate, trabecular bone, cortical bone, articular cartilage, and bone–tendon interface. Exercise also increased expression of osteogenic markers in bone and that of UCP1 in WAT, and led to bodyweight loss. Irisin intraperitoneal(IP) administration resulted in increased trabecular and cortical bone thickness and osteoblasts numbers, and concurrently induced UCP1 expression in subcutaneous WAT. Lentiviral FNDC5 IP administration increased cortical bone thickness. In vitro studies in bone cells revealed irisin increases osteoblastogenesis and mineralization, and inhibits receptor activator of nuclear factor-k B ligand(RANKL)-induced osteoclastogenesis. Taken together, our findings show that voluntary exercise increases irisin production in bone, and that an increase in circulating irisin levels enhances osteogenesis in mice. | Jin Zhang Paloma Valverde Xiaofang Zhu Dana Murray Yuwei Wu Liming Yu Hua Jiang Michel M Dard Jin Huang Zhiwei Xu Qisheng Tu Jake Chen | 2017 | Bone Research2017，5，1： | 23 |
| 18 | Transforming growth factor-β in stem cells and tissue homeostasis显示文摘TGF-β 1–3 are unique multi-functional growth factors that are only expressed in mammals, and mainly secreted and stored as a latent complex in the extracellular matrix(ECM). The biological functions of TGF-β in adults can only be delivered after ligand activation, mostly in response to environmental perturbations. Although involved in multiple biological and pathological processes of the human body, the exact roles of TGF-β in maintaining stem cells and tissue homeostasis have not been well-documented until recent advances, which delineate their functions in a given context. Our recent findings, along with data reported by others, have clearly shown that temporal and spatial activation of TGF-β is involved in the recruitment of stem/progenitor cell participation in tissue regeneration/remodeling process, whereas sustained abnormalities in TGF-β ligand activation, regardless of genetic or environmental origin, will inevitably disrupt the normal physiology and lead to pathobiology of major diseases. Modulation of TGF-β signaling with different approaches has proven effective pre-clinically in the treatment of multiple pathologies such as sclerosis/fibrosis, tumor metastasis, osteoarthritis, and immune disorders. Thus, further elucidation of the mechanisms by which TGF-β is activated in different tissues/organs and how targeted cells respond in a context-dependent way can likely be translated with clinical benefits in the management of a broad range of diseases with the involvement of TGF-β. | Xin Xu Liwei Zheng Quan Yuan Gehua Zhen Janet L.Crane Xuedong Zhou Xu Cao | 2018 | Bone Research2018，6，1： | 22 |
| 19 | Osteoclasts:New Insights显示文摘Osteoclasts,the bone-resorbing cells,play a pivotal role in skeletal development and adult bone remodeling.They also participate in the pathogenesis of various bone disorders.Osteoclasts differentiate from cells of the monocyte/macrophage lineage upon stimulation of two essential factors,the monocyte/ macrophage colony stimulating factor(M-CSF)and receptor activation of NF-кB ligand(RANKL).M-CSF binds to its receptor c-Fms to activate distinct signaling pathways to stimulate the proliferation and survival of osteoclast precursors and the mature cell.RANKL,however,is the primary osteoclast differentiation factor,and promotes osteoclast differentiation mainly through controlling gene expression by activating its receptor,RANK.Osteoclast function depends on polarization of the cell,induced by integrin αvβ3,to form the resorptive machinery characterized by the attachment to the bone matrix and the formation of the bone-apposed ruffled border.Recent studies have provided new insights into the mechanism of osteoclast differentiation and bone resorption.In particular,c-Fms and RANK signaling have been shown to regulate bone resorption by cross-talking with those activated by integrin αvβ3.This review discusses new advances in the understanding of the mechanisms of osteoclast differentiation and function. | Xu Feng Steven L.Teitelbaum | 2013 | Bone Research2013，1，1： | 20 |
| 20 | Intestinal microbiota: a potential target for the treatment of postmenopausal osteoporosis显示文摘Postmenopausal osteoporosis(PMO) is a prevalent metabolic bone disease characterized by bone loss and structural destruction, which increases the risk of fracture in postmenopausal women. Owing to the high morbidity and serious complications of PMO, many efforts have been devoted to its prophylaxis and treatment. The intestinal microbiota is the complex community of microorganisms colonizing the gastrointestinal tract. Probiotics, which are dietary or medical supplements consisting of beneficial intestinal bacteria, work in concert with endogenous intestinal microorganisms to maintain host health. Recent studies have revealed that bone loss in PMO is closely related to host immunity, which is influenced by the intestinal microbiota. The curative effects of probiotics on metabolic bone diseases have also been demonstrated. The effects of the intestinal microbiota on bone metabolism suggest a promising target for PMO management.This review seeks to summarize the critical effects of the intestinal microbiota and probiotics on PMO, with a focus on the molecular mechanisms underlying the pathogenic relationship between bacteria and host, and to define the possible treatment options. | Xin Xu Xiaoyue Jia Longyi Mo Chengcheng Liu Liwei Zheng Quan Yuan Xuedong Zhou | 2017 | Bone Research2017，5，3： | 20 |
您所在的机构暂未开通此部分的功能，请联系管理员