Results 211 to 220 of about 203,456 (311)
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
Are You a Friend or an Enemy? The Dual Action of Methylglyoxal on Brain Microvascular Endothelial Cells. [PDF]
Moisă Stoica R +5 more
europepmc +1 more source
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
Histone lactylation exacerbates acute lung injury in septic mice by promoting ferroptosis in pulmonary microvascular endothelial cells. [PDF]
Fang P +8 more
europepmc +1 more source
Investigating the Role of Type I Interferon Signaling on Muscle Disease Using Mouse Models
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
Antioxidants Trolox and Methazolamide Protect Microvascular Endothelial Cells from Oxidative Damage Induced by Sporadic and Familial Forms of Oligomeric Amyloid-β. [PDF]
Valle ML +4 more
europepmc +1 more source
Breakdown of C3 complement and IgG in peritonitis exudate-pathophysiological aspects and therapeutic approach [PDF]
Billing, A. +5 more
core
Endothelin and other mediators in the pathophysiology of portal hypertension [PDF]
Bilzer, Manfred +2 more
core +1 more source
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

