Involvement of pro-inflammatory cytokines and growth factors in the pathogenesis of Dupuytren's contracture: a novel target for a possible future therapeutic strategy?

Bianchi, Enrica; Taurone, Samanta; Bardella, Lia; Pompili, Elena; Sessa, Vincenzo; Chiappetta, Caterina; Fumagalli, Laura; Gioia, Cira Di; Pastore, Francesco Saverio; Scarpa, Susanna; Artico, Marco

doi:10.1042/cs20150088

Cited by 28 publications

(25 citation statements)

References 31 publications

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“…e innate immune response triggers proliferation of keratinocytes and release of proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin 1β, and interleukin 6 [18]. ese cytokines activate the connective tissue, leading to contractures [19]. ey also act on osteoblasts and osteoclasts, leading to the high-turnover osteoporosis and bone loss associated with CRPS [20].…”

Section: Inflammation In Pain and Role Of Autoantibodiesmentioning

confidence: 99%

Molecular Aspects of Regional Pain Syndrome

Baronio

Sadia

Paolacci

et al. 2020

Pain Research and Management

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The purpose of this review is to summarize the pathophysiology of complex regional pain syndrome (CRPS), the underlying molecular mechanisms, and potential treatment options for its management. CRPS is a multifactorial pain condition. CRPS is characterized by prolonged or excessive pain and changes in skin color and temperature, and/or swelling in the affected area, and is generally caused by stimuli that lead to tissue damage. An inflammatory response involving various cytokines and autoantibodies is generated in response to acute trauma/stress. Chronic phase pathophysiology is more complex, involving the central and peripheral nervous systems. Various genetic factors involved in the chronicity of pain have been identified in CRPS patients. As with other diseases of complex pathology, CRPS is difficult to treat and no single treatment regimen is the same for two patients. Stimulation of the vagus nerve is a promising technique being tested for different gastrointestinal and inflammatory diseases. CRPS is more frequent in individuals of 61–70 years of age with a female to male ratio of 3 : 1. Menopause, migraine, osteoporosis, and asthma all represent risk factors for CRPS and in smokers the prognosis appears to be more severe. The pathophysiological mechanisms underlying CRPS involve both inflammatory and neurological pathways. Understanding the molecular basis of CRPS is important for its diagnosis, management, and treatment. For instance, vagal nerve stimulation might have the potential for treating CRPS through the cholinergic anti-inflammatory pathway.

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Section: Inflammation In Pain and Role Of Autoantibodiesmentioning

confidence: 99%

Molecular Aspects of Regional Pain Syndrome

Baronio

Sadia

Paolacci

et al. 2020

Pain Research and Management

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“…The studies related to carpal tunnel genetic background and future therapeutic strategies are focused on cytokines and proteoglycans [19,20]. It has been reported that proinflammatory cytokines play an important role in the pathophysiology of neuropathic pain syndromes, CTS, and herniated intervertebral disks [21].…”

Section: Discussionmentioning

confidence: 99%

The Effect of IL-4 Gene Polymorphism in Carpal Tunnel Syndrome

Tekcan¹

2016

Ann Clin Anal Med

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ÖzetAmaç: Karpal tünel sendromu el bileğinde medyan sinirin disfonksiyonu ve/ veya lezyonları nedeniyle elde uyuşma ve ağrı ile karakterize nörolojik bir hastalıktır. KTS'nin patogenezi tam olarak açık olmamakla birlikte, genetik faktörler KTS'ye yatkınlıkta rol oynayabilmektedir. Sitokinler gibi biyokimyasal faktörler KTS'nin neden olduğu nöropatide rol alabilmektedir. Bu çalışma-nın amacı bir Türk populasyonunda KTS yatkınlığı ile IL-4 VNTR polimorfizmi arasındaki ilişkileri ve IL-4 VNTR polimorfizminin KTS'li hastalarda hastalığın gelişimi üzerine etkilerini incelemektir. Gereç ve Yntem: Çalışmaya KTS'li 155 hasta ve 140 sağlıklı kontrol dâhil edilmiştir. Hasta ve kontrollerin genomik DNA'lar izole edilmiş ve IL-4 geni 70 bç'lik VNTR polimorfizmleri polimeraz zincir reaksiyonu kullanılarak genotiplenmiştir. Bulgular: Hasta ve kontrol grupları arasında IL-4 genotip dağılımı açısından istatistiksel olarak anlamlı bir fark bulunmamaktadır (p>0.05). Ancak, P1 allelinin KTS'li hastalarda sağ-lıklı kontrollere göre anlamlı derecede fazla olduğu saptanmıştır (p<0.05; OR: 1.608, 95% CI: 1.05-2.44). Ayrıca, hastaların klinik özellikleri ile IL-4 genotip dağılımı arasında herhangi bir farklılık bulunmadığı belirlenmiştir. Tartışma: Bizim bulgularımız Türk populasyonunda IL-4 VNTR polimorfizminin KTS ile ilişkili bir belirteç olmadığı ve P1 allelinin ise KTS ile ilişkili olabileceğini işa-ret etmektedir. KTS'de IL-4 ve anti-inflamatuar sitokinlerin etkilerinin tespit edilmesi için daha büyük hasta populasyonu ile daha ileri çalışmaların yapıl-masına ihtiyaç bulunmaktadır. Anahtar KelimelerKarpal Tünel Sendromu, Sitokinler, İnterlökin-4, Yatkınlık Abstract Aim: Carpal tunnel syndrome (CTS) is a neurological disorder characterized by paresthesia and pain in the hands due to lesions and ⁄or dysfunction of the median nerve at the wrist. The exact pathogenesis of CTS is not clear. Genetic factors may play a role in CTS susceptibility. Biochemical mediators such as cytokines may have a role in carpal tunnel mediated neuropathy. The aim of the present study was to analyse the association of IL-4 VNTR polymorphism with CTS susceptibility and disease progression in patients with CTS in a Turkish population. Material and Method: The study included 155 patients with CTS and 140 healthy controls. Genomic DNA was isolated and genotyped using polymerase chain reaction (PCR) for the IL-4 gene 70 bp VNTR polymorphisms. Results: There was no statistically significant difference between the groups with respect to IL-4 genotype distribution (p>0.05). The P1 allele was significantly higher in CTS patients than in healthy controls (p<0.05; OR: 1.608, 95% CI: 1.05-2.44). There was no difference between IL-4 genotype distribution and clinical characteristics of patients (p>0.05). Discussion: Our findings indicate that the IL-4 70 bp VNTR polymorphism is not a relevant CTS marker and that the P1 allele may be related to CTS in a Turkish population. Further research with larger patient populations is necessary to ascertain the implications of I...

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“…Agonists of myofibroblast contraction, such as angiotensin-II, endothelin-1, and thrombin, can upregulate the expression of α-SMA [34–36]. As a result, these inflammatory cytokines play roles in myofibroblast differentiation and scar contracture [37]. …”

Section: Reviewmentioning

confidence: 99%

Current progress in understanding the molecular pathogenesis of burn scar contracture

Tan

2017

Burns &Amp; Trauma

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Abnormal wound healing is likely to induce scar formation, leading to dysfunction, deformity, and psychological trauma in burn patients. Despite the advancement of medical care treatment, scar contracture in burn patients remains a challenge. Myofibroblasts play a key role in scar contracture. It has been demonstrated that myofibroblasts, as well as inflammatory cells, fibroblasts, endothelial cells, and epithelial cells, secrete transforming growth factor-β1 (TGF-β1) and other cytokines, which can promote persistent myofibroblast activation via a positive regulation loop. In addition to the cellular contribution, the microenvironments, including the mechanical tension and integrin family, are also involved in scar contracture. Most recently, eukaryotic initiation factor 6 (eIF6), an upstream regulator of TGF-β1, has been demonstrated to be involved in myofibroblast differentiation and contraction in both in vitro fibroblast-populated collagen lattice (FPCL) and in vivo external mechanical stretch models. Moreover, the data showed that P311 could induce the transdifferentiation of epidermal stem cells to myofibroblasts by upregulating TGF-β1 expression, which mediated myofibroblast contraction. In this review, we briefly described the most current progress on the biological function of myofibroblasts in scar contracture and subsequently summarized the molecular events that initiated contracture. This would help us better understand the molecular basis of scar contracture as well as to find a comprehensive strategy for preventing/managing scar contracture.

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Involvement of pro-inflammatory cytokines and growth factors in the pathogenesis of Dupuytren's contracture: a novel target for a possible future therapeutic strategy?

Cited by 28 publications

References 31 publications

Molecular Aspects of Regional Pain Syndrome

Molecular Aspects of Regional Pain Syndrome

The Effect of IL-4 Gene Polymorphism in Carpal Tunnel Syndrome

Current progress in understanding the molecular pathogenesis of burn scar contracture

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