Transcriptional Control of Neonatal Heart Regeneration
新生儿心脏再生的转录控制
基本信息
- 批准号:10365703
- 负责人:
- 金额:$ 56.5万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2021
- 资助国家:美国
- 起止时间:2021-12-06 至 2025-11-30
- 项目状态:未结题
- 来源:
- 关键词:AdultAgeAgingCardiacCardiac MyocytesCause of DeathChromatinData SetDevelopmentDiseaseEpicardiumGene ExpressionGenesGenetic TranscriptionGlobal ChangeGoalsHeartHeart DiseasesHeart InjuriesIn VitroInjuryKnowledgeMediatingMolecularMyocardiumNatural regenerationNeonatalParacrine CommunicationPathway interactionsPlayProcessRegenerative capacityRegenerative responseTestingTimeTranscription CoactivatorTranscription RepressorTranscriptional Regulationangiogenesisbiological adaptation to stresscardiac regenerationcardiac repaircell typecytokineendoplasmic reticulum stressepigenomefunctional restorationheart functionimprovedin vivo regenerationinjuredmacrophageneonatal miceregeneration functionregeneration potentialregenerativeresponsesevere injurysingle-cell RNA sequencingtranscription factor
项目摘要
Project Summary Abstract
Heart disease remains the number one cause of death worldwide, due to the inability of the injured adult heart
to regenerate. We seek to delineate the mechanisms that govern development, disease and regeneration of the
heart and to build upon this knowledge to restore cardiac function during injury, disease and aging. In contrast
to the adult mammalian heart, which lacks regenerative capacity, the neonatal heart can efficiently regenerate
following severe injury. To explore the molecular underpinnings of neonatal cardiac regeneration, we have
analyzed global changes in gene expression and the epigenome during regeneration of the neonatal mouse
heart in comparison to later stage hearts that cannot regenerate. We have also performed single-cell RNA
sequencing of cardiomyocytes and the major non-myocyte cell types from neonatal regenerative and non-
regenerative hearts with or without injury. Integration of these comprehensive datasets has begun to reveal a
“regenerative” chromatin landscape of the heart and the transcriptional activators and repressors of this process.
The overarching goal of this project is to build upon this body of information to elucidate the mechanisms that
control the responses of the neonatal heart to injury and to harness these mechanisms to promote adult cardiac
regeneration and repair. By focusing on regenerative transcriptional circuitry and paracrine signaling
mechanisms, we intend to devise new strategies to enhance cardiomyocyte proliferation and survival,
angiogenesis and other regenerative processes mediated by various cellular constituents of the heart.
Ultimately, the molecular decoding of cardiac regeneration will provide a molecular blueprint for activating
endogenous pathways for cardiac repair and facilitate new strategies for restoring function to the injured and
aging heart.
项目摘要
心脏病仍然是世界范围内的头号死亡原因,由于受伤的成年人心脏无法
再生我们试图描绘的机制,管理发展,疾病和再生的,
心脏并利用这些知识来恢复受伤、疾病和衰老期间的心脏功能。相比之下
对于缺乏再生能力的成年哺乳动物心脏,新生儿心脏可以有效地再生
严重受伤后。为了探索新生儿心脏再生的分子基础,我们
分析了新生小鼠再生过程中基因表达和表观基因组的总体变化
与不能再生的晚期心脏相比。我们还进行了单细胞RNA
来自新生儿再生和非心肌细胞的心肌细胞和主要非心肌细胞类型的测序
有或没有损伤的再生心脏。这些综合数据集的整合已经开始揭示出
心脏的“再生”染色质景观和这一过程的转录激活因子和抑制因子。
该项目的总体目标是在此信息基础上阐明
控制新生儿心脏对损伤的反应,并利用这些机制促进成人心脏
再生和修复。通过关注再生转录回路和旁分泌信号
机制,我们打算设计新的策略来增强心肌细胞的增殖和存活,
血管生成和由心脏的各种细胞成分介导的其它再生过程。
最终,心脏再生的分子解码将为激活
内源性途径的心脏修复和促进新的战略,恢复功能的受伤,
衰老的心脏
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
RHONDA BASSEL-DUBY其他文献
RHONDA BASSEL-DUBY的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('RHONDA BASSEL-DUBY', 18)}}的其他基金
Transcriptional Control of Neonatal Heart Regeneration
新生儿心脏再生的转录控制
- 批准号:
10534778 - 财政年份:2021
- 资助金额:
$ 56.5万 - 项目类别:
Chemically assisted remodeling of infarcted heart tissue by targeting Wnt lipidation
通过靶向 Wnt 脂化化学辅助重塑梗塞心脏组织
- 批准号:
9364733 - 财政年份:2017
- 资助金额:
$ 56.5万 - 项目类别:
Deciphering the role of a novel micropeptide in cardiac function and dysfunction
破译新型微肽在心脏功能和功能障碍中的作用
- 批准号:
10331296 - 财政年份:2015
- 资助金额:
$ 56.5万 - 项目类别:
Molecular Dissection of Myoblast Fusion In Muscle Development and Regeneration
肌肉发育和再生中成肌细胞融合的分子解剖
- 批准号:
9301471 - 财政年份:2015
- 资助金额:
$ 56.5万 - 项目类别:
Deciphering the role of a novel micropeptide in cardiac function and dysfunction
破译新型微肽在心脏功能和功能障碍中的作用
- 批准号:
10089466 - 财政年份:2015
- 资助金额:
$ 56.5万 - 项目类别:
相似国自然基金
靶向递送一氧化碳调控AGE-RAGE级联反应促进糖尿病创面愈合研究
- 批准号:JCZRQN202500010
- 批准年份:2025
- 资助金额:0.0 万元
- 项目类别:省市级项目
对香豆酸抑制AGE-RAGE-Ang-1通路改善海马血管生成障碍发挥抗阿尔兹海默病作用
- 批准号:2025JJ70209
- 批准年份:2025
- 资助金额:0.0 万元
- 项目类别:省市级项目
AGE-RAGE通路调控慢性胰腺炎纤维化进程的作用及分子机制
- 批准号:
- 批准年份:2024
- 资助金额:0 万元
- 项目类别:面上项目
甜茶抑制AGE-RAGE通路增强突触可塑性改善小鼠抑郁样行为
- 批准号:2023JJ50274
- 批准年份:2023
- 资助金额:0.0 万元
- 项目类别:省市级项目
蒙药额尔敦-乌日勒基础方调控AGE-RAGE信号通路改善术后认知功能障碍研究
- 批准号:
- 批准年份:2022
- 资助金额:33 万元
- 项目类别:地区科学基金项目
补肾健脾祛瘀方调控AGE/RAGE信号通路在再生障碍性贫血骨髓间充质干细胞功能受损的作用与机制研究
- 批准号:
- 批准年份:2022
- 资助金额:52 万元
- 项目类别:面上项目
LncRNA GAS5在2型糖尿病动脉粥样硬化中对AGE-RAGE 信号通路上相关基因的调控作用及机制研究
- 批准号:n/a
- 批准年份:2022
- 资助金额:10.0 万元
- 项目类别:省市级项目
围绕GLP1-Arginine-AGE/RAGE轴构建探针组学方法探索大柴胡汤异病同治的效应机制
- 批准号:81973577
- 批准年份:2019
- 资助金额:55.0 万元
- 项目类别:面上项目
AGE/RAGE通路microRNA编码基因多态性与2型糖尿病并发冠心病的关联研究
- 批准号:81602908
- 批准年份:2016
- 资助金额:18.0 万元
- 项目类别:青年科学基金项目
高血糖激活滑膜AGE-RAGE-PKC轴致骨关节炎易感的机制研究
- 批准号:81501928
- 批准年份:2015
- 资助金额:18.0 万元
- 项目类别:青年科学基金项目
相似海外基金
The Phenomenon of Stem Cell Aging according to Methylation Estimates of Age After Hematopoietic Stem Cell Transplantation
根据造血干细胞移植后甲基化年龄估算干细胞衰老现象
- 批准号:
23K07844 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis of Age-dependent Functional Changes in Skeletal Muscle CB1 Receptors by an in Vitro Model of Aging-related Muscle Atrophy
通过衰老相关性肌肉萎缩的体外模型分析骨骼肌 CB1 受体的年龄依赖性功能变化
- 批准号:
22KJ2960 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Grant-in-Aid for JSPS Fellows
Joint U.S.-Japan Measures for Aging and Dementia Derived from the Prevention of Age-Related and Noise-induced Hearing Loss
美日针对预防与年龄相关和噪声引起的听力损失而导致的老龄化和痴呆症联合措施
- 批准号:
23KK0156 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Fund for the Promotion of Joint International Research (International Collaborative Research)
The Effects of Muscle Fatigability on Gait Instability in Aging and Age-Related Falls Risk
肌肉疲劳对衰老步态不稳定性和年龄相关跌倒风险的影响
- 批准号:
10677409 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Characterizing gut physiology by age, frailty, and sex: assessing the role of the aging gut in "inflamm-aging"
按年龄、虚弱和性别表征肠道生理学特征:评估衰老肠道在“炎症衰老”中的作用
- 批准号:
497927 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Deciphering the role of osteopontin in the aging eye and age-related macular degeneration
破译骨桥蛋白在眼睛老化和年龄相关性黄斑变性中的作用
- 批准号:
10679287 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Role of AGE/RAGEsignaling as a driver of pathological aging in the brain
AGE/RAGE信号传导作为大脑病理性衰老驱动因素的作用
- 批准号:
10836835 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Elucidation of the protein kinase NLK-mediated aging mechanisms and treatment of age-related diseases
阐明蛋白激酶NLK介导的衰老机制及年龄相关疾病的治疗
- 批准号:
23K06378 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Underlying mechanisms of age-related changes in ingestive behaviors: From the perspective of the aging brain and deterioration of the gustatory system.
与年龄相关的摄入行为变化的潜在机制:从大脑老化和味觉系统退化的角度来看。
- 批准号:
23K10845 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Targeting Age-Activated Proinflammatory Chemokine Signaling by CCL2/11 to Enhance Skeletal Muscle Regeneration in Aging
通过 CCL2/11 靶向年龄激活的促炎趋化因子信号传导以增强衰老过程中的骨骼肌再生
- 批准号:
478877 - 财政年份:2023
- 资助金额:
$ 56.5万 - 项目类别:
Operating Grants