📇 Rhumatologue · PARIS · (75) · Salarié

MME SIHAM BOLLOT-LAALAMI

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Auteur de référence en rhumatologie
33 articles scientifiques publiés — un praticien à la pointe de la recherche
Délais de RDV courts dans la région
336.2 rhumatos / 100 000 hab. — département bien doté

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📍 PARIS (75)SalariéRPPS 10000023977

✨ Génération du profil synthétique IA en cours…

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SBL OPHTALMOLOGIE
8 RUE LEO FRANKEL, 75013 PARIS
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Top publications · les plus citées

A Review of the Regulatory Challenges of Personalized Medicine

Cureus · 2024

📚 11 citations🎯 RCR 2.24Top 23% NIH🔓 Open Access📄 PDF gratuit ↗

Impact of seasonal cycle on rheumatoid arthritis based on genetic and epigenetic mechanisms

Frontiers in immunology · 2025

📚 3 citations🔓 Open Access📄 PDF gratuit ↗

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Rheumatoid arthritis is an autoimmune disease characterized by chronic inflammation and progressive joint destruction. Genetic and environmental risk factors contribute to the development of rheumatoid arthritis (RA). Among environmental factors, seasonal cycles are reported to impact the clinical phenotypes in RA, with rheumatic flares being aggravated during the winter season. Gaining insight into the seasonal effects on molecular drivers can be vital in resolving seasonal cycles in RA pathogenesis. To understand this phenomenon, genome-wide association study (GWAS) and candidate genes were reviewed to identify their role in susceptibility to RA. Subsequently, it was verified how many of these genes are modulated by seasonal influences. Furthermore, the role of epigenetic modifications, such as DNA methylation and non-coding RNAs, involved in RA pathogenesis and whether these epigenetic effects are also impacted by seasonal fluctuation were examined. Finally, it was investigated how these genetic and epigenetic mechanisms result in the breakdown of self-tolerance and the initiation of an autoimmune action. Upon overlapping the genetic and epigenetic observations influenced by seasonal cycles, it was evident that seasonal cycles do impact the genetic and epigenetic machinery, which possibly can explain the reasons for seasonal flares in RA pathogenesis. The evidence indicates that genetic and epigenetic mechanisms are driven by climatic variation and that the timing and duration of the aberrant expression of immune response genes will drive the autoantibodies to develop seasonal flares of RA.

Gene expression analysis reveals mir-29 as a linker regulatory molecule among rheumatoid arthritis, inflammatory bowel disease, and dementia: Insights from systems biology approach

PloS one · 2025

📚 3 citations🔓 Open Access📄 PDF gratuit ↗

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Background Rheumatoid arthritis (RA) is a degenerative autoimmune disease, often managed through symptomatic treatment. The co-occurrence of the reported extra-articular comorbidities such as inflammatory bowel disease (IBD), and dementia may complicate the pathology of the disease as well as the treatment strategies. Therefore, in our study, we aim to elucidate the key genes, and regulatory elements implicated in the progression and association of these diseases, thereby highlighting the linked potential therapeutic targets. Methodology Ten microarray datasets each for RA, and IBD, and nine datasets for dementia were obtained from Gene Expression Omnibus. We identified common differentially expressed genes (DEGs) and constructed a gene-gene interaction network. Subsequently, topology analysis for hub gene identification, cluster and functional enrichment, and regulatory network analysis were performed. The hub genes were then validated using independent microarray datasets from Gene Expression Omnibus. Results A total of 198 common DEGs were identified from which CD44, FN1, IGF1, COL1A2, and POSTN were identified as the hub genes in our study. These hub genes were mostly enriched in significant processes and pathways like tissue development, collagen binding, cell adhesion, regulation of ERK1/2 cascade, PI3K-AKT signaling, and cell surface receptor signaling. Key transcription factors TWIST2, CEBPA, EP300, HDAC1, HDAC2, NFKB1, RELA, TWIST1, and YY1 along with the miRNA hsa-miR-29 were found to regulate the expression of the hub genes significantly. Among these regulatory molecules, miR-29 emerged as a significant linker molecule, bridging the molecular mechanisms of RA, IBD, and dementia. Validation of our hub genes demonstrated a similar expression trend in the independent datasets used for our study. Conclusion Our study underscores the significant role of miR-29 in modulating the expression of hub genes and the associated transcription factors, which are crucial in the comorbidity status of RA, dementia, and IBD. This regulatory mechanism highlights miR-29 as a key player in the pathogenesis of these comorbid diseases.

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MME SIHAM BOLLOT-LAALAMI

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Top publications · les plus citées

Publications scientifiques (33) — classées par pathologie

Case report / série11

Pédiatrie6

Transversal6

Revue générale5

csDMARDs1

Économie santé1

Épidémiologie & registres1

Essai clinique1

Génétique1

Gériatrie1

IRM ostéo-articulaire1

Lupus1

Pharmacovigilance1

Revue / méta-analyse1

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