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Abstract：
Ehlers-Danlos syndromes (EDSs) constitute a heterogeneous group of connective tissue disorders characterized by joint hypermobility, skin hyperextensibility, and tissue fragility. Asymptomatic EDSs, joint hypermobility without associated syndromes, EDSs, and hypermobility spectrum disorders are the commonest phenotypes associated with joint hypermobility. Joint hypermobility syndrome (JHS) is a connective tissue disorder characterized by extreme flexibility of the joints, along with pain and other symptoms. JHS can be a sign of a more serious underlying genetic condition, such as EDS, which affects the cartilage, bone, fat, and blood. The exact cause of JHS could be related to genetic changes in the proteins that add flexibility and strength to the joints, ligaments, and tendons, such as collagen. Membrane proteins are a class of proteins embedded in the cell membrane and play a crucial role in cell signaling, transport, and adhesion. Dysregulated membrane proteins have been implicated in a variety of diseases, including cancer, cardiovascular disease, and neurological disorders; recent studies have suggested that membrane proteins may also play a role in the pathogenesis of JHS. This article presents an exploration of the causative factors contributing to musculoskeletal pain in individuals with hypermobility, based on research findings. It aims to provide an understanding of JHS and its association with membrane proteins, addressing the clinical manifestations, pathogenesis, diagnosis, and management of JHS.
摘要：
Ehlers-Danlos综合征（EDS）构成了一组以关节过度活动为特征的异质结缔组织疾病，皮肤过度伸展性，组织脆弱.无症状EDS,没有相关综合征的关节过度活动，EDS,和高迁移率谱系障碍是与关节高迁移率相关的最常见的表型。关节过度活动综合征（JHS）是一种结缔组织疾病，其特征是关节的极端柔韧性，还有疼痛和其他症状。JHS可能是更严重的潜在遗传病的征兆，例如EDS，影响软骨，骨头,脂肪，还有血.JHS的确切原因可能与蛋白质的遗传变化有关，这些蛋白质增加了关节的灵活性和强度，韧带,和肌腱，如胶原蛋白。膜蛋白是一类包埋在细胞膜上的蛋白质，在细胞信号传导中起着至关重要的作用，运输,和附着力。失调的膜蛋白与多种疾病有关，包括癌症,心血管疾病,和神经系统疾病；最近的研究表明，膜蛋白也可能在JHS的发病机理中起作用。本文探讨了导致活动过度的人肌肉骨骼疼痛的致病因素，基于研究结果。它旨在提供对JHS及其与膜蛋白的关联的理解，解决临床表现，发病机制，诊断,和JHS的管理。
