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Results for “Cicatrix, Hypertrophic”

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At least 19 recordsLinked to original sources
PubMed2026

Deciphering miRNA-mediated genetic architecture of immune cell subsets in hypertrophic scars and keloids: A 2-step Mendelian randomization study unveiling causal associations.

This study aimed to investigate the potential causal roles of specific circulating microRNAs (miRNAs) and immune cell subsets in the pathogenesis of hypertrophic scars and keloids using a 2-step Mendelian randomization framework. We employed a 2-sample Mendelian randomization approach to evaluate the causal relationships between miRNAs, immune cell genotypes, and scar phenotypes. The analysis integrated miRNA expression quantitative trait loci, immune cell genome-wide association studies, and scar datasets. A 2-step mediation analysis was conducted to assess the indirect effects of miRNAs on scars through immune cell genotypes, using inverse variance weighted methods and complementary sensitivity analyses to ensure robustness. Our analysis identified significant associations between specific miRNAs and scar phenotypes. Notably, miR-6887-5p exhibited a total effect on keloid formation risk (β = 0.324, 95% confidence interval [CI]: 0.073-0.576) and a direct effect (β = 0.283, 95% CI: 0.027, 0.538), with a marginally significant mediation effect through B-cell activating factor receptor on CD20- CD38- B cells (β = 0.042, 95% CI: -0.001, 0.084, P = .047). For hypertrophic scars, miR-345-5p demonstrated a significant total effect (β = -0.501, 95% CI: -0.903, -0.099) and direct effect (β = -0.469, 95% CI: -0.872, -0.066), with a significant mediation effect through CD28+ CD45RA- CD8dim T cell percentage (β = -0.032, 95% CI: -0.062, -0.002, P = .034). miR-4801 showed a significant total effect (β = -0.246, 95% CI: -0.429, -0.064) and direct effect (β = -0.218, 95% CI: -0.402, -0.033), with a marginally significant mediation effect through T cell absolute count (β = -0.028, 95% CI: -0.057, -0.000, P = .043). These findings highlight the interplay between miRNAs and immune cell subsets in scar pathogenesis. This study provides preliminary evidence for the causal roles of specific miRNAs and immune cell subsets in scar formation, emphasizing the potential of miRNA-immune cell axes as therapeutic targets. While the identified associations offer important insights into the molecular mechanisms of scar heterogeneity, further validation through mechanistic studies and clinical trials is necessary to translate these genetic insights into clinical interventions.

Humans↗
PubMed2026

Systemic Comorbidities of Keloid and Hypertrophic Scars: A Phenome-Wide Association Study in a Multiethnic U.S. Pediatric Cohort.

BACKGROUND: Excessive scarring (ES), including keloids and hypertrophic scars, impairs function, appearance, and quality of life in children. Its pediatric comorbidity spectrum is not well defined, limiting anticipatory guidance and multidisciplinary care. This research aims to investigate comorbidities of ES in a diverse pediatric cohort using a phenome-wide association study (PheWAS). METHODS: This population-based study leveraged longitudinal electronic health record (EHR) data from participants enrolled in the Children's Hospital of Philadelphia (CHOP) from 2006. Diagnosis codes (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9-CM] and Tenth Revision [ICD-10-CM]) were mapped to 3109 phenotype codes (PheCodes). PheWAS analyses were conducted using logistic regression, with Bonferroni correction applied to account for multiple testing. RESULTS: Among 86,092 pediatric participants, 662 (0.77%) were identified with ES; the remaining served as controls. Multivariable PheWAS screening identified 154 significant associations across 16 disease categories, of which 105 were not reported previously to our knowledge. Dermatologic phenotypes (n = 28; 18%) were most enriched, including acne and other follicular disorders, eczema, pigmentary changes, papulosquamous and granulomatous disorders, and cutaneous infections. Respiratory phenotypes (n = 21; 14%) included respiratory failure, pneumonia, asthma, allergic rhinitis, pharyngitis, and tonsillar hypertrophy. Sense organ disorders (n = 19; 12%) comprised conjunctivitis, refractive errors, otitis, and hearing impairment. Infection-related phenotypes (n = 14; 9%) highlighted susceptibility to viral (influenza, human papillomavirus [HPV], molluscum contagiosum), fungal (candidiasis, dermatophytosis), and bacterial infections. CONCLUSIONS: These findings suggest that ES in children indicates not only localized wound-healing impairment, but also systemic immune, developmental, and proliferative dysregulations, emphasizing the need for genetic and mechanistic studies to clarify causal pathways and multidisciplinary surveillance beyond dermatologic care.

Humans↗
PubMed1979

Histopathological types of cardiac fibrosis in myocardial disease.

Myocardial fibrosis is a frequently observed pathologic finding. It is a common practice to differentiate macroscopic scarring and microscopic scarring, but there has been little attempt to distinguish the various types of interstitial fibrosis, and to determine their prevalence in different cardiac disorders. In this study, we have semiquantitatively assessed microscopic scarring, interfibre and perivascular fibrosis and a distinctive type of plexiform fibrosis. We examined ten hearts with congestive cardiomyopathy, ten with hypertrophic cardiomyopathy, ten with severe valvular aortic stenosis and ten normal hearts. Perivascular and interfibre fibrosis were quantitatively closely linked and most marked in the congestive cardiomyopathy and the valvular aortic stenosis groups. Plexiform fibrosis occurred maximally in the hypertrophic obstructive cardiomyopathy group, closely associated with myocardium exhibiting muscle fibre disarray. Our study demonstrates that although different types of interstitial fibrosis have particular associations with certain disease entities, the associations are not specific. The recognition of the prevalence of one or more types of interstitial fibrosis may, however, assist in the histopathologic diagnosis of certain myocardial disorders.

Adult↗
PubMed1978

Camouflaging scars in the head and neck area.

Any break in the continiuty of healthy skin results in the formation of a scar. The way the scar is formed and the factors affecting the final appearance are discussed. Basic surgical principles as they relate to the revision of scars and the different surgical techniques used for revising scars are presented. Surgical adjuncts used following scar revision and hypertrophic scars and keloids and their treatment are also discussed.

Cicatrix↗
PubMed1975

Collagen polymorphism in human scars.

Collagen similar to the collagen found in embryonic skin (same intermolecular cross-links and same structure of the polypeptide chains) is synthesized in young human scars. Later on, in normal scars, this collagen is replaced by the collagen of adult skin progressively. In contrast, in hypertrophic scars, a high proportion of collagen of "embryonic" type is present permanently. In granulation tissues of chronic inflammation, experimentally developed in rats, similar "embryonic" collagen has been found ; these granuloma are proposed as a model in laboratory animals of human hypertrophic scars.

Animals↗