In primary Sjögren syndrome (pSS), chronic inflammation of exocrine glands results in tissue destruction and sicca symptoms, primarily of the mouth and eyes. Fatigue, arthralgia and myalgia are also common symptoms, whereas extraglandular manifestations that involve the respiratory, nervous and vascular systems occur in a subset of patients. The disease predominantly affects women, with an estimated female to male ratio of 14 to 1. The aetiology of pSS, however, remains incompletely understood, and effective treatment is lacking. Large-scale genetic and epigenetic investigations have revealed associations between pSS and genes in both innate and adaptive immune pathways. The genetic variants mediate context-dependent effects, and both sex and environmental factors can influence the outcome. As such, genetic and epigenetic studies can provide insight into the dysregulated molecular mechanisms, which in turn might reveal new therapeutic possibilities. This Review discusses the genetic and epigenetic features that have been robustly connected with pSS, putting them into the context of cellular function, carrier sex and environmental challenges. In all, the observations point to several novel opportunities for early detection, treatment development and the pathway towards personalized medicine.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10010657 | PMC |
http://dx.doi.org/10.1038/s41584-023-00932-6 | DOI Listing |
Front Oncol
January 2025
Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Introduction: Small cell lung cancer (SCLC) is characterized by significant heterogeneity and plasticity, contributing to its aggressive progression and therapy resistance. Autophagy, a conserved cellular process, is implicated in many cancers, but its role in SCLC remains unclear.
Methods: Using a genetically engineered mouse model ( ; ; GFP-LC3-RFP-LC3△G), we tracked autophagic flux to investigate its effects on SCLC biology.
Front Cell Dev Biol
January 2025
Developmental Epigenetics Laboratory, Department of Animal Science, Reproductive and Developmental Sciences Program, Michigan State University, East Lansing, MI, United States.
Hemasphere
January 2025
Université Paris Cité, Institut Cochin, INSERM U1016, CNRS UMR8104 Assistance Publique-Hôpitaux de Paris.Centre, Laboratory of Hematology, Hôpital Cochin Paris France.
Lower risk (LR) myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem and progenitor disorders caused by the accumulation of somatic mutations in various genes including epigenetic regulators that may produce convergent DNA methylation patterns driving specific gene expression profiles. The integration of genomic, epigenomic, and transcriptomic profiling has the potential to spotlight distinct LR-MDS categories on the basis of pathophysiological mechanisms. We performed a comprehensive study of somatic mutations and DNA methylation in a large and clinically well-annotated cohort of treatment-naive patients with LR-MDS at diagnosis from the EUMDS registry (ClinicalTrials.
View Article and Find Full Text PDFFront Bioinform
January 2025
RNA Bioinformatics and High Throughput Analysis, Friedrich Schiller University Jena, Jena, Germany.
Cell-cell communication mediated by ligand-receptor interactions (LRI) is critical to coordinating diverse biological processes in homeostasis and disease. Lately, our understanding of these processes has greatly expanded through the inference of cellular communication, utilizing RNA extracted from bulk tissue or individual cells. Considering the challenge of obtaining tissue biopsies for these approaches, we considered the potential of studying cell-free RNA obtained from blood.
View Article and Find Full Text PDFEnviron Epigenet
January 2025
Institute of Human Genetics, School of Medicine, Pontificia Universidad Javeriana, Bogotá 110231, Colombia.
Fine particulate matter (PM), an atmospheric pollutant that settles deep in the respiratory tract, is highly harmful to human health. Despite its well-known impact on lung function and its ability to exacerbate asthma, the molecular basis of this effect is not fully understood. This integrated transcriptomic and epigenomic data analysis from publicly available datasets aimed to determine the impact of PM exposure and its association with asthma in human airway epithelial cells.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!