Nuclear Factor-κB Activation as a Pathological Mechanism of Lipid Metabolism and Atherosclerosis
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作者:
Yu, Xiao-Hua
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Univ South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R ChinaUniv South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R China
Yu, Xiao-Hua
[1
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Zheng, Xi-Long
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Univ Calgary, Hlth Sci Ctr, Cumming Sch Med, Dept Biochem & Mol Biol,Libin Cardiovasc Inst Alb, Calgary, AB, CanadaUniv South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R China
Zheng, Xi-Long
[2
]
Tang, Chao-Ke
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Univ South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R ChinaUniv South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R China
Tang, Chao-Ke
[1
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机构:
[1] Univ South China, Key Lab Atherosclerol Hunan Prov, Mol Target New Drug Discovery & Cooperat Innovat, Life Sci Res Ctr, Hengyang, Peoples R China
Atherosclerosis is a chronic inflammatory disease of the arterial wall with lipid-laden lesions, involving a complex interaction between multiple different cell types and cytokine networks. Inflammatory responses mark all stages of atherogenesis: from lipid accumulation in the intima to plaque formation and eventual rupture. One of the most important regulators of inflammation is the transcription factor nuclear factor-kappa B (NF-kappa B), which is activated through the canonical and noncanonical pathways in response to various stimuli. NF-kappa B has long been regarded as a proatherogenic factor, because it is implicated in multiple pathological processes during atherogenesis, including foam cell formation, vascular inflammation, proliferation of vascular smooth muscle cells, arterial calcification, and plaque progression. In contrast, inhibition of NF-kappa B signaling has been shown to protect against atherosclerosis. This chapter aims to discuss recent progress on the roles of NF-kappa B in lipid metabolism and atherosclerosis and also to highlight its potential therapeutic benefits.
机构:
JFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan
Natl Canc Ctr, Res Inst, Div Pathol, Tokyo 104, JapanJFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan
Yasuda, Jun
Nakanishi, Kazuaki
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Natl Canc Ctr, Res Inst, Div Pathol, Tokyo 104, Japan
Hokkaido Univ, Grad Sch Med, Dept Gen Surg, Sapporo, Hokkaido, JapanJFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan
Nakanishi, Kazuaki
Chuma, Makoto
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Natl Canc Ctr, Res Inst, Div Pathol, Tokyo 104, Japan
Hokkaido Univ, Grad Sch Med, Dept Gastroenterol, Sapporo, Hokkaido, JapanJFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan
Chuma, Makoto
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Kamiyama, Toshiya
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Todo, Satoru
Hirohashi, Setsuo
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Natl Canc Ctr, Res Inst, Div Pathol, Tokyo 104, JapanJFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan
Hirohashi, Setsuo
Sakamoto, Michiie
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Natl Canc Ctr, Res Inst, Div Pathol, Tokyo 104, Japan
Keio Univ, Sch Med, Dept Pathol, Tokyo 160, JapanJFCR Canc Inst, Dept Cell Biol, Koto Ku, Tokyo 1358550, Japan