Cartilage tissue engineering for obesity-induced osteoarthritis: Physiology, challenges, and future prospects.

Cartilage tissue engineering for obesity-induced osteoarthritis: Physiology, challenges, and future prospects.
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DOI:
10.1016/j.jot.2020.07.004
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发表时间:
2021-01
影响因子:
6.6
通讯作者:
Zhang P
Zhang P
中科院分区:
医学2区
文献类型:
--
作者:
Sun AR;Udduttula A;Li J;Liu Y;Ren PG;Zhang P

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骨关节炎(OA)是一种多因素关节疾病,其病理变化影响整个关节组织。肥胖被认为是最有影响力的风险因素的开始和进展的OA在承重和非承重关节。肥胖诱导的OA是一个新定义的表型组,其中慢性低度炎症起着核心作用。除了持续的慢性炎症外,由于负重关节上体重增加导致的异常机械负荷也是肥胖诱导的OA发生和进展的原因。目前OA的治疗方法仍在不断发展。基于组织工程的软骨再生策略是近年来最有前途的治疗突破之一。然而,由于异常的机械需求、改变的细胞生物力学和生化活性、持续的慢性炎症和其他肥胖相关因素,患有肥胖诱导的OA的患者通常被排除在软骨修复尝试之外。随着全球肥胖人群数量的惊人增加,需要一种能够有效修复和恢复受损滑膜关节的创新治疗方法,这对这一患者亚群至关重要。在这篇综述中,我们讨论了肥胖诱导的OA中全身和局部炎症反应的参与,以及改变机械负荷对滑膜关节病理变化的影响。此外,我们研究了软骨组织工程的当前策略,并解决了基于细胞的OA治疗的关键挑战。此外,我们提供了创新的方法和潜在的策略,以克服在治疗肥胖引起的OA的障碍的例子。总之,这篇综述提供了对肥胖引起的OA的深入了解,并为肥胖引起的OA的组织工程治疗提供了未来的研究方向。
Osteoarthritis (OA) is a multifactorial joint disease with pathological changes that affect whole joint tissue. Obesity is acknowledged as the most influential risk factor for both the initiation and progression of OA in weight-bearing and non-weight-bearing joints. Obesity-induced OA is a newly defined phenotypic group in which chronic low-grade inflammation has a central role. Aside from persistent chronic inflammation, abnormal mechanical loading due to increased body weight on weight-bearing joints is accountable for the initiation and progression of obesity-induced OA. The current therapeutic approaches for OA are still evolving. Tissue-engineering-based strategy for cartilage regeneration is one of the most promising treatment breakthroughs in recent years. However, patients with obesity-induced OA are often excluded from cartilage repair attempts due to the abnormal mechanical demands, altered biomechanical and biochemical activities of cells, persistent chronic inflammation, and other obesity-associated factors. With the alarming increase in the number of obese populations globally, the need for an innovative therapeutic approach that could effectively repair and restore the damaged synovial joints is of significant importance for this sub-population of patients. In this review, we discuss the involvement of the systemic and localized inflammatory response in obesity-induced OA and the impact of altered mechanical loading on pathological changes in the synovial joint. Moreover, we examine the current strategies in cartilage tissue engineering and address the critical challenges of cell-based therapies for OA. Besides, we provide examples of innovative ways and potential strategies to overcome the obstacles in the treatment of obesity-induced OA. Altogether, this review delivers insight into obesity-induced OA and offers future research direction on the creation of tissue engineering-based therapies for obesity-induced OA.
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