T‐bet transcription factor in cardiovascular disease: Attenuation or inflammation factor?

Haybar, Habib; Rezaeeyan, Hadi; Shahjahani, Mohammad; Shirzad, Reza; Saki, Najmaldin

doi:10.1002/jcp.27935

Cited by 12 publications

(6 citation statements)

References 62 publications

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“…The Th1 lineage-specific transcription factor T-bet, a member of the of the T box family, promotes Th1 differentiation [353] by binding to the IFN-γ promoter, stimulating IFN-γ production [354]. T-bet deficiency slows atherosclerosis development and increases production of the atheroprotective Th2 cytokines IL-4, IL-5, and IL-10, and IgM antibodies [346].…”

Section: Adaptive Immunitymentioning

confidence: 99%

Immunobiology of Atherosclerosis: A Complex Net of Interactions

Herrero‐Fernández

Gómez-Bris

Somovilla-Crespo

et al. 2019

IJMS

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Cardiovascular disease is the leading cause of mortality worldwide, and atherosclerosis the principal factor underlying cardiovascular events. Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction, intimal lipid deposition, smooth muscle cell proliferation, cell apoptosis and necrosis, and local and systemic inflammation, involving key contributions to from innate and adaptive immunity. The balance between proatherogenic inflammatory and atheroprotective anti-inflammatory responses is modulated by a complex network of interactions among vascular components and immune cells, including monocytes, macrophages, dendritic cells, and T, B, and foam cells; these interactions modulate the further progression and stability of the atherosclerotic lesion. In this review, we take a global perspective on existing knowledge about the pathogenesis of immune responses in the atherosclerotic microenvironment and the interplay between the major innate and adaptive immune factors in atherosclerosis. Studies such as this are the basis for the development of new therapies against atherosclerosis. Int. J. Mol. Sci. 2019, 20, 5293 2 of 48 cytotoxic T lymphocytes at the interface between innate and adaptive immunity. Abundant evidence indicates that innate and adaptive immunity both play important roles in the onset and progression of atherosclerosis [1][2][3]. For example, Csf1 −/− mice, which lack macrophage colony stimulating factor (M-CSF, also known as CSF1) are less prone to developing atherosclerosis [4]. Moreover, mice lacking B and T cells (Rag1 −/− or Rag2 −/− mice lacking recombination-activating genes 1 or 2 or mice carrying the severe combined immunodeficiency (SCID) mutation) are resistant to atherosclerosis in the presence of mild hypercholesterolemia [5][6][7][8][9][10]. Int. J. Mol. Sci. 2019, 20, 5293 2 of 46 cells are cytotoxic T lymphocytes at the interface between innate and adaptive immunity. Abundant evidence indicates that innate and adaptive immunity both play important roles in the onset and progression of atherosclerosis [1][2][3]. For example, Csf1 −/− mice, which lack macrophage colony stimulating factor (M-CSF, also known as CSF1) are less prone to developing atherosclerosis [4]. Moreover, mice lacking B and T cells (Rag1 −/− or Rag2 −/− mice lacking recombination-activating genes 1 or 2 or mice carrying the severe combined immunodeficiency (SCID) mutation) are resistant to atherosclerosis in the presence of mild hypercholesterolemia [5-10]. Atherosclerosis's PathophysiologyAtherosclerosis is a chronic inflammatory disease of large and medium-sized arteries [20], characterized by endothelial dysfunction and the accumulation of low-density lipoproteins (LDL), immune cells, and necrotic debris in the subendothelial space, resulting in the formation of an atherosclerotic plaque [21][22][23][24]. LDL deposition is more likely in regions with turbulent flow and low shear stress [25] sensed by the vascular endothelium [26]. Turbulent flow modulates endothelial transcrip...

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Section: Adaptive Immunitymentioning

confidence: 99%

Immunobiology of Atherosclerosis: A Complex Net of Interactions

Herrero‐Fernández

Gómez-Bris

Somovilla-Crespo

et al. 2019

IJMS

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“…The most common pathogeneses of CVDs are inflammatory processes (Ruparelia et al, 2017). Various transcription factors are related to inflammatory responses in CVDs such as T-bet (Haybar et al, 2019), signal transducer and activator of transcription 3 (STAT3) (Kurdi et al, 2018), interferon regulatory factors (IRFs), activator protein 1 (AP-1) (Smale and Natoli, 2014), and transcription factor Bcl11b (Daher et al, 2019). However, the key player in the regulation of inflammation is the transcription factor nuclear factor kappa B (NFκB) (Van Der Heiden et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Flavonoids as Natural Anti-Inflammatory Agents Targeting Nuclear Factor-Kappa B (NFκB) Signaling in Cardiovascular Diseases: A Mini Review

et al. 2019

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Cardiovascular diseases (CVDs) such as angina, hypertension, myocardial ischemia, and heart failure are the leading causes of morbidity and mortality worldwide. One of the major transcription factors widely associated with CVDs is nuclear factor-kappa B (NFκB). NFκB activation initiates the canonical and non-conical pathways that promotes activation of transcription factors leading to inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. Flavonoids are bioactive polyphenolic compounds found abundantly in various fruits, vegetables, beverages (tea, coffee), nuts, and cereal products with cardiovascular protective properties. Flavonoids can be classified into six subgroups based on their chemical structures: flavanones, flavones, flavonols, flavan-3-ols, isoflavones, and anthocyanidins. As NFκB inhibitors, these flavonoids may modulate the expression of pro-inflammatory genes leading to the attenuation of the inflammatory responses underlying various cardiovascular pathology. This review presents an update on the anti-inflammatory actions of flavonoids via inhibition of NFκB mechanism supporting the therapeutic potential of these natural compounds in various CVDs.

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“…Cardiovascular disease (CVD) is an aggressive disease with a high morbidity rate worldwide [1][2][3]. Excessive oxidative stress and abnormal inflammatory responses accumulate endothelial cell (EC (ECs) injury [4]. The initial step of CVD is EC dysfunction-induced cardiac microvascular injury [5,6].…”

Section: Introductionmentioning

confidence: 99%