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|Type:||Artigo de periódico|
|Title:||A hypothesis for the anti-inflammatory and mechanotransduction molecular mechanisms underlying acupuncture tendon healing|
|Author:||de Almeida, MD|
de Oliveira, LP
|Abstract:||A previous study demonstrated that acupuncture increases the synthesis and reorganisation of collagen molecules in rat tendons after injury. Clinical studies have shown that acupuncture improves pain and functional activity in patients with tendinopathy. However, the molecular mechanisms underlying these effects are unknown. Recent studies have shown that acupuncture can modulate both anti-inflammatory (AI) and mechanotransduction (MT) molecular pathways. Moreover, the modulation of these pathways can increase type I collagen synthesis, which is the main factor that influences tendon biomechanical properties. Our hypothesis is that acupuncture increases synthesis and subsequent reorganisation of type I collagen during tendon healing by concomitant modulation of the Toll-like receptor-nuclear factor-kappa B AI pathway, the mitogen-activated protein kinases pathway and the Rho/Rac-F-actin MT pathway. Increased collagen synthesis and reorganisation requires that at least one acupoint is anatomically connected with the site of the injury because of the local tenoblast MT mechanism. Confirmation of this hypothesis will increase the knowledge of acupuncture modulation of the previously mentioned molecular pathways, and such confirmation may also help to establish the relationships between the different types of acupuncture needle stimulation and the influence of acupuncture stimuli on pathway activity levels. In addition, the downstream therapeutic effects of acupuncture therapy may be established. This hypothesis can be verified in a rat tendon healing model, and subsequent clinical protocols for tendon healing can be developed and evaluated as standalone therapies or as a component of a combination therapy.|
|Editor:||Bmj Publishing Group|
|Appears in Collections:||Artigos e Materiais de Revistas Científicas - Unicamp|
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