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The transcription factor Miz1-mediated mechanism of lung aging

转录因子Miz1介导的肺衰老机制

基本信息

批准号：
10198018
负责人：
JING LIU
金额：
$ 49.03万
依托单位：
UNIVERSITY OF ILLINOIS AT CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-03-15 至 2023-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10198018
关键词：
Age Aging Alveolar Macrophages Animals Cause of Death Cell Aging Cell Cycle Cell Cycle Arrest Cell Cycle Inhibition Cells Characteristics Chronic Chronic Obstructive Airway Disease Chronic lung disease Complex Data Development Embryo Epigenetic Process Epithelial Epithelial Cells Gene Expression Genes Growth Factor HDAC1 gene Human Immunology In Vitro Inflammation Inflammatory Knockout Mice Lead Link Lung Mass Spectrum Analysis Mediating Molecular Mus Nature Paper Pathogenesis Pathology Pathway interactions Patients Peptide Hydrolases Pharmaceutical Preparations Phenotype Production Proteins Pulmonary Emphysema Pulmonary Inflammation Reporter Reporting Repression Risk Factors Role Tissues Transcriptional Activation Tumor Suppression Zinc Fingers age related chemokine chromatin remodeling cytokine differential expression effective therapy experimental study genetic corepressor genome wide association study genomic locus inhibitor/antagonist insight loss of function normal aging novel therapeutics prevent programs recruit senescence therapeutic target transcription factor transcriptome sequencing

项目摘要

Project Summary/Abstract Chronic obstructive pulmonary disease (COPD) has risen to the third leading cause of death in the US and specific and effective therapies are not available. Age is the most important risk factor for COPD. The mechanisms of age-related changes that lead to COPD pathogenesis are poorly understood. In this proposal, we will study whether Miz1 epigenetically represses NF-B-dependent components of senescence-associated secretory phenotype (SASP), which acts in cooperation with inhibition of cell cycle arrest to suppress the senescence program, thereby preventing the development of COPD. Completion of this proposal, which includes animal and human studies, will provide fundamental insights into the pathogenesis of COPD and thus provide therapeutic targets.

项目总结/摘要慢性阻塞性肺疾病（COPD）已上升为美国第三大死亡原因，没有具体有效的治疗方法。年龄是COPD最重要的危险因素。的导致COPD发病机制的年龄相关变化的机制知之甚少。在这一提议中，我们将研究Miz 1是否在表观遗传学上抑制衰老相关的NF-κ B依赖性成分，分泌表型（SASP），其与细胞周期阻滞的抑制合作，以抑制细胞周期的变化。衰老计划，从而防止COPD的发展。完成本提案，其中包括动物和人类研究，将提供对COPD发病机制的基本见解，治疗目标