title: Interferon-γ in foam cell formation and progression of atherosclerosis.
abstract: Interferon-γ (IFN-γ), the sole member in type II IFN predominantly secreted by macrophages and T cells, is a critical regulator of immune function and provides a robust first line of defense against invading pathogens. Binding of IFN-γ to its receptor complex can activate a variety of downstream signaling pathways, particularly the Janus kinase (JAK)/signal transducer and activator of transcription (STAT), to induce gene transcription within the target cells. This pro-inflammatory mediator is highly expressed in atherosclerotic lesions and promotes foam cell formation, but its effects on the atherogenesis are complex, with both pro- and anti-atherogenic properties. IFN-γ also contributes to the development of myocardial infarction and stroke, the two main atherosclerotic diseases. Inhibition of IFN-γ signaling may prevent the development of atherosclerosis and help treat atherosclerotic diseases. Since IFN-γ may also exert anti-atherogenic effects, the safety and efficacy of anti-IFN-γ treatment still require careful evaluation in the clinical setting. In the current review, we summarize recent progression on regulation and signaling pathways of IFN-γ, and highlight its roles in foam cell formation, atherosclerosis, myocardial infarction as well as stroke. An increased understanding of these processes will help to develop novel IFN-γ-centered therapies for atherosclerotic diseases.
authors.affiliation: Life Science Research Center, Key Laboratory for Atherosclerology of Hunan Province, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan 421001, China.
authors.forename: Xiao-Hua
authors.initials: XH
authors.lastname: Yu
authors.affiliation: Department of Spine, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Biochemistry and Molecular Biology, The Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, The University of Calgary, Health Sciences Center, 3330 Hospital Dr NW, Calgary, Alberta T2N 4 N1, Canada.
authors.forename: Xi-Long
authors.initials: XL
authors.lastname: Zheng
authors.affiliation: Department of Pediatrics, The First Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China. Electronic address: 2117149447@qq.com.
authors.forename: Yun-Hua
authors.initials: YH
authors.lastname: Yang
authors.affiliation: Life Science Research Center, Key Laboratory for Atherosclerology of Hunan Province, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan 421001, China. Electronic address: tangchaoke@qq.com.
authors.forename: Chao-Ke
authors.initials: CK
authors.lastname: Tang
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology*; D018450:Disease Progression; D005487:Foam Cells / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D007371:Interferon-gamma
keywords: Atherosclerosis; Foam cells; IFN-γ; Myocardial infarction; Stroke