TL;DR
The study suggests a shared inflammatory and immune-mediated transcriptomic program linking AMI and PD, and identifies FCN1 and LYN as candidate shared immune markers.
HLA-G, HLA-A, HLA-C, and B2M modulate macrophage and T cell functions, driving immune dysregulation in AS, highlighting the potential of these molecules as diagnostic biomarkers and therapeutic targets.
This integrated computational and experimental study identifies a set of high-value diagnostic core genes in AMI and validates the specific upregulation of novel genes (GPR97, PROK2) in myocardial ischemia, placing them within a pathological network involving metabolic, immune and protective pathways.
The findings suggest that CCL4 may serve as a potential diagnostic biomarker for AMI, and the observed immune-metabolic associations provide a basis for future mechanistic and translational studies.
This study reveals shared aging-related genes, pathways, and immune cell dysregulation between PD and RA, elucidating how aging exacerbates both diseases through immune-inflammatory mechanisms.
These results nominate CLEC4A and P2RY13 as candidate genes potentially involved in shared APS–CAS immune-related pathways, with expression changes associated with CAS progression among APS patients.
SIGLEC1 and TRIM25 are context-dependent immune signatures in sepsis and SLE, with loss-of-function evidence supporting SIGLEC1 in macrophage inflammatory responses, and both genes exhibited potential discriminatory capacity between disease cohorts and healthy controls.
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