Unlabelled: Chronic tendinopathy is a debilitating tendon disorder with disappointing treatment outcomes. This review focuses on the potential roles of chronic low-grade inflammation in promoting tendinopathy in obesity. A systematic literature search was performed to identify all clinical studies supporting the actions of obesity-associated inflammatory mediators in the development of tendinopathy. The mechanisms of obesity-induced chronic inflammation in adipose tissue are firstly reviewed. Common inflammatory mediators potentially linking obesity and the development of tendinopathy, and their association with mechanical overuse, are discussed, along with pre-clinical evidences and a systematic literature search on clinical studies. The potential contribution of local adipose tissues in the promotion of inflammation, pain and tendon degeneration is then discussed. The future research directions are proposed.
Translational Potential Statement: Better understanding of the roles of obesity-associated inflammatory mediators on tendons will clarify the pathophysiological drivers of tendinopathy in patients with obesity and identify possible treatment targets. Further studies on the mechanisms of obesity-induced chronic inflammation on tendon are a promising direction for the treatment of tendinopathy.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8666605 | PMC |
http://dx.doi.org/10.1016/j.jot.2021.10.003 | DOI Listing |
Front Biosci (Landmark Ed)
December 2024
Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, 400016 Chongqing, China.
Background: Acute lung injury (ALI) significantly impacts the survival rates in intensive care units (ICU). Releasing a lot of pro-inflammatory mediators during the progression of the disease is a core feature of ALI, which may lead to uncontrolled inflammation and further damages the tissues and organs of patients. This study explores the potential therapeutic mechanisms of Dexmedetomidine (Dex) in ALI.
View Article and Find Full Text PDFJ Integr Neurosci
December 2024
Department of Neurology, Hainan West Central Hospital, 571799 Danzhou, Hainan, China.
Background: Ischemic stroke (IS) is the leading cause of mortality worldwide. Herein, we aimed to identify novel biomarkers and explore the role of C-type lectin domain family 7 member A () in IS.
Methods: Differentially expressed genes (DEGs) were screened using the GSE106680, GSE97537, and GSE61616 datasets, and hub genes were identified through construction of protein-protein interaction networks.
J Integr Neurosci
December 2024
Cerebral Palsy Center in Neurosurgery, Second Affiliated Hospital of Xinjiang Medical University, 830063 Urumqi, Xinjiang, China.
Cerebral palsy (CP), a common neurological disorder in children, remains a significant research focus. The interleukin (IL) family, pivotal mediators in inflammatory responses, shows increased expression in various neuroinflammatory diseases, markedly influencing their onset and progression. Elevated IL levels in the brains of children with CP, in contrast to healthy peers, reflect similar elevations in neurological conditions linked to CP, indicating a strong association between CP and the IL family.
View Article and Find Full Text PDFJ Inflamm Res
December 2024
Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, People's Republic of China.
Introduction: Systemic lupus erythematosus is a heterogeneous autoimmune disease. A burst of autoimmune reactions in various systems can lead to severe clinical conditions closely associated with mortality. T cells serve as mediators that drive the occurrence and maintenance of inflammatory processes.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Pathology, First Clinical Hospital, Harbin Medical University, Harbin, China.
Microglial-mediated neuroinflammation is crucial in the pathophysiological mechanisms of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). Mitochondria are central regulators of inflammation, influencing key pathways such as alternative splicing, and play a critical role in cell differentiation and function. Mitochondrial ATP synthase coupling factor 6 (ATP5J) participates in various pathological processes, such as cell proliferation, migration, and inflammation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!