Results 211 to 220 of about 203,456 (311)

Molecular Stratification of Antiphospholipid Syndrome Through Integrative Analysis of the Whole‐Blood RNA Transcriptome

open access: yesArthritis &Rheumatology, EarlyView.
Objective Antiphospholipid syndrome (APS) is a thromboinflammatory disorder characterized by clinical and mechanistic heterogeneity that complicates early diagnosis and hinders targeted treatment. We aimed to identify distinct molecular endotypes among antiphospholipid antibody (aPL)–positive patients using whole‐blood transcriptomics.
Amala Ambati   +13 more
wiley   +1 more source

A Cooperative Release of Mitochondrial DNA From Platelets and Neutrophils Drives an Interferon Signature in Systemic Sclerosis

open access: yesArthritis &Rheumatology, EarlyView.
Objective Mitochondria are organelles with a hypomethylated circular genome. Mitochondrial DNA (mtDNA) in the systemic circulation has been implicated in inflammation. This study investigates the role of circulating DNA in systemic sclerosis (SSc) and the cellular mechanisms governing its release.
Stavros Giaglis   +9 more
wiley   +1 more source

Investigating the Role of Type I Interferon Signaling on Muscle Disease Using Mouse Models

open access: yesArthritis &Rheumatology, EarlyView.
Objective Dysregulated type I interferon (IFN) signaling contributes to autoimmune myositis pathogenesis. We investigated the therapeutic effects of JAK inhibitors in two mouse models. We also examined how type I IFNs affect muscle vasculature. Methods Myositis was induced in major histocompatibility complex class I double transgenic ([TRE‐H‐2Kb (H ...
Rita Spathis   +11 more
wiley   +1 more source

Breakdown of C3 complement and IgG in peritonitis exudate-pathophysiological aspects and therapeutic approach [PDF]

open access: yes, 1988
Billing, A.   +5 more
core  

TWEAK/Fn14 signaling drives oxidative cardiac injury in systemic lupus erythematosus: Evidence from patient biomarker studies, lupus mouse models, and cardiomyocyte assays

open access: yesArthritis &Rheumatology, Accepted Article.
Objective Cardiac involvement is a major cause of morbidity in systemic lupus erythematosus (SLE). Tumor necrosis factor–like weak inducer of apoptosis (TWEAK) is elevated in SLE, but its contribution to lupus‐associated cardiac injury is unclear. We investigated the role of TWEAK/Fn14 signaling in SLE‐related cardiomyopathy and its potential as a ...
Yale Liu   +12 more
wiley   +1 more source

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