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Adipokines: New Therapeutic Target for Osteoarthritis?

ABSTRACT: PURPOSE OF THE REVIEW:Osteoarthritis (OA) is an aging-associated and injury-induced joint disease characterized by cartilage degradation, bone sclerosis, and persistent low-grade inflammation in the joint. Aging and injury are triggers of joint pathological changes mediated by pro-inflammatory factors, some of which are secreted by white adipose tissue. Adipokines including adiponectin, leptin, resistin, chemerin, IL-6, and TNF-? are major players not only during inflammation but also in metabolic regulation of joint cells including chondrocytes, osteoblasts, osteoclasts as well as mesenchymal stem cells. The purpose of this review is to summarize the signal transduction pathways of adipokines in the articular joint to provide new information on potential targets for intervention of OA. RECENT FINDINGS:The risk of knee osteoarthritis is associated with adipokine gene polymorphism. While the infrapatellar fat pad is a major source of adipokines in knee synovial fluid, adipocytes also accumulate in the bone marrow during aging and obesity. Adipokines can act as SASPs (senescence associated secretory phenotype factors) that participate in cellular senescence of chondrocytes, but they also regulate energy metabolism impacting bone remodeling. Thus, adipokines are closely related to the metabolic syndrome and degenerative pathological changes in cartilage and bone during OA. Modulating the effects of adipokines on different cell types in the intra-articular joint will be a promising new option for OA intervention.

SUBMITTER: Xie C

PROVIDER: S-EPMC7291783 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Adipokines: New Therapeutic Target for Osteoarthritis?

Xie Chenxi C Chen Qian Q

Current rheumatology reports 20191207 12

<h4>Purpose of the review</h4>Osteoarthritis (OA) is an aging-associated and injury-induced joint disease characterized by cartilage degradation, bone sclerosis, and persistent low-grade inflammation in the joint. Aging and injury are triggers of joint pathological changes mediated by pro-inflammatory factors, some of which are secreted by white adipose tissue. Adipokines including adiponectin, leptin, resistin, chemerin, IL-6, and TNF-α are major players not only during inflammation but also in ...[more]

PMID: 31813080

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Project description:Astrocytes and neurons dynamically interact during physiological processes, and it is now widely accepted that they are both organized in plastic and tightly regulated networks. Astrocytes are connected through connexin-based gap junction channels, with brain region specificities, and those networks modulate neuronal activities, such as those involved in sleep-wake cycle, cognitive, or sensory functions. Additionally, astrocyte domains have been involved in neurogenesis and neuronal differentiation during development; they participate in the "tripartite synapse" with both pre-synaptic and post-synaptic neurons by tuning down or up neuronal activities through the control of neuronal synaptic strength. Connexin-based hemichannels are also involved in those regulations of neuronal activities, however, this feature will not be considered in the present review. Furthermore, neuronal processes, transmitting electrical signals to chemical synapses, stringently control astroglial connexin expression, and channel functions. Long-range energy trafficking toward neurons through connexin-coupled astrocytes and plasticity of those networks are hence largely dependent on neuronal activity. Such reciprocal interactions between neurons and astrocyte networks involve neurotransmitters, cytokines, endogenous lipids, and peptides released by neurons but also other brain cell types, including microglial and endothelial cells. Over the past 10 years, knowledge about neuroglial interactions has widened and now includes effects of CNS-targeting drugs such as antidepressants, antipsychotics, psychostimulants, or sedatives drugs as potential modulators of connexin function and thus astrocyte networking activity. In physiological situations, neuroglial networking is consequently resulting from a two-way interaction between astrocyte gap junction-mediated networks and those made by neurons. As both cell types are modulated by CNS drugs we postulate that neuroglial networking may emerge as new therapeutic targets in neurological and psychiatric disorders.

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Adipokines: New Therapeutic Target for Osteoarthritis?

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Adipokines: New Therapeutic Target for Osteoarthritis?

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