Innate Immunity Metabolism and Vascular Injury
Innate Immunity Metabolism and Vascular Injury
批准号:
8635912
负责人:
DAVID L. WOODLAND
金额:
$1.5万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2014
资助国家:
美国
项目状态:
已结题
起止时间:
2014-03-15 至 2015-03-14
关键词:
Adipose tissueApoptosisApoptoticAreaAtherosclerosisBiologyBlood VesselsBritish ColumbiaCanadaCardiovascular DiseasesCellsChronicCollaborationsComplementComplications of Diabetes MellitusCoronary ArteriosclerosisDevelopmentEnvironmentFatty acid glycerol estersFutureGenomicsGoalsImmune systemInflammationInflammatory ResponseInjuryInsulin ResistanceInvestigationKnowledgeLipidsMacrophage ActivationMediatingMetabolicMetabolic DiseasesMetabolic stressMetabolismMethodologyModalityMorbidity - disease rateMyeloid CellsNatural ImmunityNecrosisNon-Insulin-Dependent Diabetes MellitusObesityOutcomeParticipantPathway interactionsPostdoctoral FellowResearchResearch PersonnelScientistStudentsSystems BiologyTechniquesTherapeuticTissuesTrainingclinical practicedisease mechanisms studyimprovedinterdisciplinary approachmacrophagemeetingsmonocytemortalitynew therapeutic targetpublic health relevancesymposiumtraffickingvascular bedvascular inflammation
中文摘要
点击翻译按钮获取中文摘要
英文摘要
ABSTRACT
Support is requested for a Keystone Symposia meeting entitled Innate Immunity, Metabolism and Vascular
Injury, organized by Ajay Chawla, Peter Tontonoz and Gwendalyn J. Randolph. The meeting will be held in
Whistler, British Columbia, Canada from March 23-28, 2014. A chronic low-grade inflammatory response is a
defining feature of various cardiovascular and metabolic diseases, including atherosclerosis, obesity, and type
2 diabetes. This smoldering inflammation in tissues, whether it is in the vascular bed, white adipose tissue or
perivascular fat, is primarily mediated by the innate immune system. Consequently, this meeting will bring
together leading investigators in areas of macrophage biology, vascular inflammation, atherosclerosis, and
obesity-induced metabolic disease. Sessions will encompass a broad range of topics highlighting the
importance of and mechanisms by which innate immunity contributes to progression of cardiovascular and
metabolic diseases, including monocyte development and trafficking, macrophage activation in vascular bed
and adipose tissues, and systems biology of myeloid cells. Exciting new developments in sensing of metabolic
stress by inflammasomes, clearance of apoptotic cells by macrophages, and initiation of necrotic cell death
programs will also be discussed. These basic studies will be complemented by talks discussing new strategies
for promoting plaque regression, and targeting innate inflammation to treat insulin resistance, type 2 diabetes,
and coronary artery disease. Opportunities for interdisciplinary interactions will be significantly enhanced by
the concurrent meeting on Complications of Diabetes, which will share a two plenary sessions with this
meeting.
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