Reprogramming Interferon Regulatory Factor Signaling in Cardiometabolic Diseases

Zhang, Yaxing; Li, Hongliang

doi:10.1152/physiol.00038.2016

Cited by 24 publications

(18 citation statements)

References 126 publications

(143 reference statements)

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“…In hepatocytes, PRR‐elicited intracellular signaling can activate or coregulate the transcription of nuclear transcription factors (IRF, NF‐κB, peroxisome proliferator‐activated receptor [PPAR]‐α, stearoyl‐CoA desaturase‐1, etc.) and modulate intrahepatic inflammation and broad metabolic profiles …”

Section: Parenchymal Cells Of the Liver With Immune Functionsmentioning

confidence: 99%

“…and modulate intrahepatic inflammation and broad metabolic profiles. (51)(52)(53)(66)(67)(68)(69)(70) Eicosanoids, such as prostaglandins (PGs), thromboxanes (TXs), and leukotrienes (LTs), are wellknown mediators of inflammation responses. (71) Cyclooxegenase (COX) is a critical enzyme in the pathway that leads to formation of PGs and TXs from arachidonic acid (AA).…”

Section: Hepatocytesmentioning

confidence: 99%

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The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis

2019

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Inflammation and metabolic dysfunction are hallmarks of nonalcoholic steatohepatitis (NASH), which is one of the fastest‐growing liver diseases worldwide. Emerging evidence indicates that innate immune mechanisms are pivotal drivers of inflammation and other pathological manifestations observed in NASH, such as hepatosteatosis, insulin resistance (IR), and fibrosis. This robust innate immune reaction is intrinsic to the liver, which is an important immunological organ that contains a coordinated network of innate immune cells, including Kupffer cells (KCs), dendritic cells (DCs), and lymphocytes. Hepatocytes and liver sinusoidal endothelial cells (LSECs) are not formally innate immune cells, but they take on immune cell function when stressed. These cells can sense excess metabolites and bacterial products and translate those signals into immune responses and pathological hepatic changes during the development of NASH. In this review, we take a historical perspective in describing decades of research that aimed to identify the key molecular and cellular players in the innate immune system in the setting of NASH. Furthermore, we summarize the innate immune cells that are involved in the progression of NASH and illustrate how they sense disturbances in circulating metabolic factors by innate immune receptors and subsequently initiate the intercellular signaling cascades that lead to persistent inflammation and progression of hepatic complications.

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Section: Parenchymal Cells Of the Liver With Immune Functionsmentioning

confidence: 99%

Section: Hepatocytesmentioning

confidence: 99%

The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis

2019

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“…[120] TRAF1 and TRAF6 can be utilized to promote the activation of ASK1 whereas deubiquitinase TNFa-induced protein 3 (TNFAIP3), dickkopf-3 (DKK3), CASP8 and FADD-like apoptosis regulator (CFLAR), cellular repressor of E1A-stimulated genes (CREG) and caspase recruitment domain 6 can suppress ASK1 activation, which improves the NASH. [111,115,[134][135][136] Different types of IRFs play various roles. Cylindromatosis (CYLD), ubiquitin-specific protease 18 (USP18), and dual-specificity phosphatase 14 (DUSP14) are reported to be candidate enzymes for suppressing the progression of NASH via inhibiting TAK1, [92,[128][129][130] whereas the E3 ligase tripartite motif 8, TRAF3, promotes NASH.…”

Section: Inflammation and Innate Immunitymentioning

confidence: 99%

Insights into the Epidemiology, Pathogenesis, and Therapeutics of Nonalcoholic Fatty Liver Diseases

et al. 2018

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Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease which affects ≈25% of the adult population worldwide, placing a tremendous burden on human health. The disease spectrum ranges from simple steatosis to steatohepatitis, fibrosis, and ultimately, cirrhosis and carcinoma, which are becoming leading reasons for liver transplantation. NAFLD is a complex multifactorial disease involving myriad genetic, metabolic, and environmental factors; it is closely associated with insulin resistance, metabolic syndrome, obesity, diabetes, and many other diseases. Over the past few decades, countless studies focusing on the investigation of noninvasive diagnosis, pathogenesis, and therapeutics have revealed different aspects of the mechanism and progression of NAFLD. However, effective pharmaceuticals are still in development. Here, the current epidemiology, diagnosis, animal models, pathogenesis, and treatment strategies for NAFLD are comprehensively reviewed, emphasizing the outstanding breakthroughs in the above fields and promising medications in and beyond phase II.

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“…The increased production of endothelin-1 (ET-1), Ang II, catecholamines and pro-inflammatory cytokines activate their cognate receptors and downstream signaling events, which lead to cardiomyocytes necrosis, apoptosis, autophagy, or hypertrophy; and promote fibroblast activation to produce collagen and other proteins that cause fibrosis [35-37]. Recently, we and others have shown that H 2 can prevent various heart diseases through blocking parts of these molecular and cellular signaling events described above (Table 2).…”

Section: The Effects Of H2 In Heart Diseasesmentioning

confidence: 99%

Hydrogen Therapy in Cardiovascular and Metabolic Diseases: from Bench to Bedside

Zhang

Tan

et al. 2018

Cell Physiol Biochem

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Hydrogen (H₂) is colorless, odorless, and the lightest of gas molecules. Studies in the past ten years have indicated that H₂ is extremely important in regulating the homeostasis of the cardiovascular system and metabolic activity. Delivery of H₂ by various strategies improves cardiometabolic diseases, including atherosclerosis, vascular injury, ischemic or hypertrophic ventricular remodeling, intermittent hypoxia- or heart transplantation-induced heart injury, obesity and diabetes in animal models or in clinical trials. The purpose of this review is to summarize the physical and chemical properties of H₂, and then, the functions of H₂ with an emphasis on the therapeutic potential and molecular mechanisms involved in the diseases above. We hope this review will provide the future outlook of H₂-based therapies for cardiometabolic disease.

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Reprogramming Interferon Regulatory Factor Signaling in Cardiometabolic Diseases

Cited by 24 publications

References 126 publications

The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis

The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis

Insights into the Epidemiology, Pathogenesis, and Therapeutics of Nonalcoholic Fatty Liver Diseases

Hydrogen Therapy in Cardiovascular and Metabolic Diseases: from Bench to Bedside

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