Ye et al. reveal that BAK is an interferon-stimulated gene up-regulated by the STAT1-IRF1 axis during viral infection, which induces mitochondria-derived inflammation. This mechanism is utilized by RNA and DNA viruses and underlies inflammatory diseases.

Psoriasis is an autoimmune skin disease, and its pathogenesis remains incompletely understood. As central drivers of psoriasis pathogenesis that bridge innate and adaptive immunity, macrophages are known to be modulated in their function by insulin-induced gene 1 (INSIG1), a regulator of cholesterol synthesis. Bioinformatic analysis of human psoriatic lesions reveals a significant negative correlation between INSIG1 expression and pro-inflammatory cytokine levels (IL-23, IL-17A). Single-cell RNA sequencing (scRNA-seq) and immunofluorescence confirm significantly reduced INSIG1 expression specifically in macrophages from psoriatic skin. In vivo, myeloid-specific Insig1 deficiency exacerbates imiquimod (IMQ)-induced psoriasiform dermatitis, characterized by increased epidermal thickening and immune infiltration. By activating sterol regulatory element-binding protein 2 (SREBP2), INSIG1 deficiency leads to the transcriptional upregulation of STAT1, which drives M1 macrophage polarization

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Liang et al. identify an NAD+-responsive adipokine Serpina3n that protects skeletal muscle against aging- and disease-associated atrophy. NAD+ elevation promotes adipose Serpina3n production through STAT1, and Serpina3n promotes skeletal muscle protein homeostasis and metabolic adaptation through pyruvate carboxylase, revealing an endocrine mechanism linking adipose NAD+ metabolism to muscle health.

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Read the full paper: Dysferlin promotes inflammatory macrophage responses and modulates Ca2+-dependent STAT1 signaling

Iglesias-Herrero et al. longitudinally assess JAK-inhibitor treatment response in two patients with STAT1 gain-of-function and show that it induces rapid b