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Mechanisms underlying caloric restriction-mediated resolution of atherosclerosis

热量限制介导的动脉粥样硬化解决机制

基本信息

批准号：
10677793
负责人：
Ada Weinstock
金额：
$ 24.9万
依托单位：
UNIVERSITY OF CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-08-05 至 2025-07-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10677793
关键词：
Adipose tissue Affect Apoptosis Arterial Fatty Streak Arteries Atherosclerosis Blood Vessels Body Weight decreased Bone Marrow Caloric Restriction Cardiovascular Diseases Cardiovascular system Cause of Death Cell physiology Cells Cholesterol Chronic Circulation Data Development Diet Disease Disease Management Disease remission Emigrations Epigenetic Process Event Foundations Future Genetic Transcription Hematopoietic Hematopoietic System Hematopoietic stem cells High Fat Diet Human Immune Immunologics Inflammation Inflammatory Kinetics Macrophage Mediating Medical Metabolic Diseases Modification Molecular Morbidity - disease rate Mus Obese Mice Obesity Pathology Pathway interactions Phagocytosis Phase Phenotype Population Postdoctoral Fellow Process Proliferating Research Resolution Risk Factors Role Signal Transduction Testing Time Tissues Transplantation Work bone comorbidity efficacious intervention hematopoietic cell transplantation hypercholesterolemia monocyte mortality mouse model novel obesity development progenitor programs recruit single-cell RNA sequencing systemic inflammatory response

项目摘要

PROJECT SUMMARY Obesity and atherosclerosis are frequently comorbid conditions contributing to substantial morbidity and mortality worldwide. The processes are characterized by inflammation in the adipose tissue and vasculature, respectively, that share many pathophysiologic pathways. Although processes underlying obesity and atherosclerosis-related inflammation are well studied, the signals that promote disease resolution and remission are largely unknown, especially in the context of concomitant inflammation resolution. As a postdoctoral fellow, I investigated how resolution of obesity-related inflammation influences cardiovascular disease and found that caloric-restriction- induced weight loss in obese mice promotes resolution of atherosclerosis. Building upon these exciting findings, I propose in Aim 1 to evaluate the impact of caloric-restriction on obese adipose tissue and hematopoietic progenitors and whether the pro-resolving phenotype produced by to caloric-restriction can be transferred through adipose or hematopoietic cell transplantation. In Aim 2, I propose to investigate the mechanisms by which caloric-restriction influences the content and composition of atherosclerotic lesions and promotes atherosclerosis resolution. This work will reveal novel functions of cells and tissues that influence the atherosclerotic process in weight loss. Additionally, these studies will identify novel molecular pathways that may be targeted for the concomitant treatment of adipose tissue and atherosclerosis-related inflammation.

项目总结