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Fibrosis is a common pathological state characterized by the excessive accumulation of extracellular matrix components, but the pathogenesis of the disease is still not clear. Previous studies have shown that microRNA-29 (miR-29) can play pivotal roles in the regulation of a variety of organ fibrosis, including cardiac fibrosis, hepatic fibrosis, lung fibrosis, systemic sclerosis, and keloid. In this review, we outline the structure, expression, and regulation of miR-29 as well as its role in fibrotic diseases. [ABSTRACT FROM AUTHOR]

Keloid scarring is a dermal fibroproliferative response characterized by excessive and progressive deposition of collagen; aetiology and molecular pathology underlying keloid formation and progression remain unclear. Genetic predisposition is important in the pathogenic processes of keloid formation, however, environmental factors and epigenetic mechanisms may also play pivotal roles. Epigenetic modification is a recent area of investigation in understanding the molecular pathogenesis of keloid scarring and there is increasing evidence that epigenetic changes may play a role in induction and persistent activation of fibroblasts in keloid scars. Here we have reviewed three epigenetic mechanisms: DNA methylation, histone modification and the role of non-coding RNAs. We also review the evidence that these mechanisms may play a role in keloid formation - in future, it may be possible that epigenetic markers may be used instead of prognostic or diagnostic markers here. However, there is a significant amount of work required to increase our current understanding of the role of epigenetic modification in keloid disease. [ABSTRACT FROM AUTHOR]

Melanoma is a common skin cancer associated with ultraviolet light exposure and genetic variance. However, the etiology and molecular mechanisms of melanoma remain unknown. Recent studies have shown that microRNAs (miRNAs) can play key roles in the development and prognosis of this disease. In this study, we reviewed several pivotal miRNAs that may contribute to melanoma by involvement in the processes of invasion, migration, and metastasis of melanoma cells. [ABSTRACT FROM AUTHOR]

Abstract: Background: Some studies suggested that Glutathione S-transferases M1/T1(GSTM1/T1) null polymorphisms may be associated with the risk of vitiligo. Aims: The purpose of this study is to further evaluate the association between GSTM1/T1 null polymorphisms and the susceptibility to vitiligo. Methods: We carried out a retrieval of studies in the databases. Odds ratios (OR) and 95% confidence intervals (95% CIs) were used to assess the strength of this association. We analyzed the data using Stata 11.0. Results: Six case–control studies including 1358 cases and 1673 controls were included in this meta-analysis. Our overall results showed the GSTM1 or GSTT1 null polymorphism was associated with vitiligo (GSTM1:OR=1.59, 95% CI: 1.21–2.08, P=0.001; GSTT1: OR=1.30, 95% CI: 1.12–1.51, P=0.001). In the subgroup analysis, the GSTM1 null polymorphism might be a genetic risk factor to vitiligo in East Asian (OR=1.71, 95% CI: 1.12–2.63, P=0.014) but not in the Mediterranean, however individuals with the GSTT1 null polymorphism in the Mediterranean (OR=1.76, 95% CI: 1.15–2.71, P=0.010) but not in East Asian have a greater predisposition to vitiligo. In addition there was also a significant trend toward an association with the combination of the GSTM1 null and GSTT1 null in either East Asians or Mediterraneans. Conclusion: The GSTM1/T1 null polymorphisms may be associated with vitiligo. More studies are needed to confirm this conclusion. [Copyright &y& Elsevier]

Background: Catechol-O-methyltransferase (COMT) gene has been reported to be associated with the risk of Parkinson's disease (PD).Aims: To evaluate the associations of PD risk with COMT polymorphisms.Materials and Methods: A retrieval of studies that investigated associations between COMT polymorphisms and PD was carried out. Studies were included if they met the eligibility criteria.Statistical Analysis: Data were analyzed using Stata version 12.0.Results: A total of 18 studies including 2926 PD cases and 3151 controls were included. The results showed no significant association with all genotypes and alleles in Caucasians. However in Asians, the homozygote A/A (Odds ratio [OR] =1.51, 95% confidence interval [CI] =1.16-1.98, P =0.002) tends to increase risk of PD, however, the homozygote G/A (OR =0.85, 95% CI =0.74-0.98, P =0.03) may be a slightly protective effect against PD.Conclusions: This study showed that the COMT polymorphisms may be associated with PD in Asians rather than Caucasians. But further studies are needed to confirm our results. [ABSTRACT FROM AUTHOR]

In previous study, we have found the catechol- O-methyltransferase (COMT) Val158Met polymorphism may be associated with the risk of Parkinson's disease (PD) in Asians, especially Japanese population. In this study, we further evaluated the associations of PD wearing-off susceptibility with COMT polymorphisms. We carried out a retrieval of studies and included the relevant studies which met the criteria. After the data were extracted, the Stata software 11.0 was used to analyse the genotype frequencies. A total of five studies were included. The pooled result indicated that genotype AA was significantly associated with the wearing-off risk of PD (AA vs. others: OR = 2.52, 95 % CI 1.21-5.26, P = 0.013; AA vs. GA: OR = 2.51, 95 % CI 1.18-5.34, P = 0.017; AA vs. GG: OR = 2.17, 95 % CI 1.09-4.33, P = 0.027). The results also showed allele A was correlated with PD wearing-off risk (A vs. G: OR = 1.95, 95 % CI 1.18-3.22, P = 0.009). In conclusion, this study suggested that Val158Met polymorphisms in COMT may increase the risk of wearing-off. Further studies with larger sample sizes are needed to confirm our results. [ABSTRACT FROM AUTHOR]

Background and Aims: Several studies have shown that the apolipoprotein E (ApoE) gene is associated with the development of psoriasis. However, there is a controversy. The aim of the present study was to evaluate the association of psoriasis risk with ApoE polymorphisms. Methods: We carried out a systematic search of studies that explored associations between ApoE polymorphisms and psoriasis. The genotype distribution of the control group in each study was calculated to determine whether or not there was compliance with the Hardy-Weinberg equilibrium. Overall effect sizes were assessed by odds ratio (OR) with 95% confidence intervals (CI). The selection to use the random-effects model or fixed-effects model depended on the size of the heterogeneity among the included studies. The fail-safe number (Nfs) was used to test the potential publication bias. We analyzed the data using Stata v.10.0. Results: A total of seven studies with 966 patients and 1,086 controls were included. The results indicated that the ε2 allele was associated with increased risk of psoriasis (ε2 vs. ε3+ε4: OR = 1.47, 95% CI = 1.23–1.75, p <0.05), whereas the ε3 allele and ε3/ε3 genotype may decrease risk of psoriasis (OR = 0.71, 95% CI = 0.62–0.82, p <0.05; OR = 0.63, 95% CI = 0.52–0.77, p <0.05, respectively). In the subgroup analysis according to ethnicity, the increased risk of psoriasis remained in the Asian and European populations, whereas no significant association was found in other populations for other polymorphisms. Conclusions: Our study suggests that the ApoE polymorphisms are associated with the risk of psoriasis, especially ε2 and ε3 alleles. Further studies are needed to confirm our results. [Copyright &y& Elsevier]