Turnover of Musculotendinous Collagen Following Exercise
运动后肌腱胶原蛋白的周转
基本信息
- 批准号:6880300
- 负责人:
- 金额:$ 0.28万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2004
- 资助国家:美国
- 起止时间:2004-05-01 至 2004-06-30
- 项目状态:已结题
- 来源:
- 关键词:Scandinavian countryclinical researchcollagenconnective tissue developmentconnective tissue metabolismexercisehuman subjectkneemalemicrodialysismuscle metabolismmusculoskeletal systempostdoctoral investigatorprotein metabolismradiotracerrepetitive motion injurysports injurytendon injurytendonsyoung adult human (21-34)
项目摘要
DESCRIPTION (provided by applicant): Overuse injuries are common to those regularly performing activity as well as those with job related injuries. The site of failure in chronic overuse injuries are often musculotendinous structures. The most abundant component of musculotendinous tissue is collagen. Despite its ubiquity, collagen tissue is not well understood and is perceived to be rather inert. However, evidence is accumulating that collagen is quite dynamic. The purpose of this proposal is to further elucidate the processes of muscle and tendon collagen synthesis and degradation in response to mechanical loading and its deficiencies in overuse injuries. Specifically it is hypothesized that, 1) muscle and tendon collagen increase synthesis in response to exercise but these rates do not follow the same time course, 2) rates of muscle and tendon collagen degradation increase in response to exercise, 3) in subjects with an overuse tendon injury, rates of collagen synthesis in tendon (but not muscle) are transiently decreased compared to healthy tendon after an acute bout of exercise. To this end muscle collagen synthesis and degradation and its regulation will be studied with a combination of stable isotope tracers, tissue sampling, microdialysis, and molecular biology techniques during recovery from a strenuous bout of exercise in healthy subjects and those with patellar tendonitis. With elucidation of the patterns of collagen synthesis and degradation and where deficiencies lie in those with injuries, it will then be possible to design specific interventions to aid in restructuring.
描述(由申请人提供):过度使用伤害对于那些经常进行活动以及因工作受伤的人来说很常见。慢性过度使用损伤的失效部位通常是肌肉肌腱结构。肌腱组织最丰富的成分是胶原蛋白。尽管胶原组织无处不在,但人们对它的了解还不是很多,并且被认为是相当惰性的。然而,越来越多的证据表明胶原蛋白是非常活跃的。该提案的目的是进一步阐明肌肉和肌腱胶原蛋白合成和降解的过程,以响应机械负荷及其在过度使用损伤中的缺陷。具体来说,假设:1)肌肉和肌腱胶原蛋白的合成因运动而增加,但这些速率并不遵循相同的时间进程,2)肌肉和肌腱胶原蛋白的降解速率因运动而增加,3)在过度使用肌腱损伤的受试者中,与健康肌腱相比,在剧烈运动后,肌腱(而非肌肉)中胶原蛋白的合成速率短暂降低。为此,将结合稳定同位素示踪剂、组织取样、微透析和分子生物学技术,在健康受试者和患有髌腱炎的受试者从剧烈运动恢复期间研究肌肉胶原蛋白的合成和降解及其调节。通过阐明胶原蛋白合成和降解的模式以及受伤者的缺陷所在,就可以设计具体的干预措施来帮助重建。
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 }}
Benjamin Francis Miller其他文献
Benjamin Francis Miller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('Benjamin Francis Miller', 18)}}的其他基金
Mechanism through which chronically elevated mTOR activity impairs aged muscle recovery after disuse atrophy
长期升高的 mTOR 活性损害废用性萎缩后老年肌肉恢复的机制
- 批准号:
10641855 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
Mechanism through which chronically elevated mTOR activity impairs aged muscle recovery after disuse atrophy
长期升高的 mTOR 活性损害废用性萎缩后老年肌肉恢复的机制
- 批准号:
10473096 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
Determining the context specificity of metformin treatment on muscle mitochondria and healthspan
确定二甲双胍治疗对肌肉线粒体和健康寿命的背景特异性
- 批准号:
10462944 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
Dissecting the integrated mechanisms of protein turnover to prevent proteostatic decline with aging
剖析蛋白质周转的综合机制,以防止蛋白质沉积随衰老而下降
- 批准号:
10390925 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
Dissecting the integrated mechanisms of protein turnover to prevent proteostatic decline with aging
剖析蛋白质周转的综合机制,以防止蛋白质沉积随衰老而下降
- 批准号:
10706458 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
Determining the context specificity of metformin treatment on muscle mitochondria and healthspan
确定二甲双胍治疗对肌肉线粒体和健康寿命的背景特异性
- 批准号:
10596174 - 财政年份:2022
- 资助金额:
$ 0.28万 - 项目类别:
DNA turnover in myofibers is an unrecognized mechanism for maintaining skeletal muscle health
肌纤维中的 DNA 更新是维持骨骼肌健康的一种未被认识的机制
- 批准号:
10239252 - 财政年份:2020
- 资助金额:
$ 0.28万 - 项目类别:
A novel approach to understand a mechanism of proteostatic decline with aging
一种理解衰老过程中蛋白质抑制下降机制的新方法
- 批准号:
10229298 - 财政年份:2020
- 资助金额:
$ 0.28万 - 项目类别:
DNA turnover in myofibers is an unrecognized mechanism for maintaining skeletal muscle health
肌纤维中的 DNA 更新是维持骨骼肌健康的一种未被认识的机制
- 批准号:
10065144 - 财政年份:2020
- 资助金额:
$ 0.28万 - 项目类别:
Does insulin sensitivity impact the potential of metformin to slow aging?
胰岛素敏感性是否会影响二甲双胍延缓衰老的潜力?
- 批准号:
10579890 - 财政年份:2019
- 资助金额:
$ 0.28万 - 项目类别:
相似海外基金
Pulmonary impairment after tuberculosis in Georgia: Enhancing clinical research capacity to address the intersection of non-communicablediseases and tuberculosis
格鲁吉亚结核病后的肺损伤:增强临床研究能力以解决非传染性疾病和结核病的交叉问题
- 批准号:
10002119 - 财政年份:2019
- 资助金额:
$ 0.28万 - 项目类别:
BRITTLE BONE DISORDERS CONSORTIUM OF THE RARE DISEASE CLINICAL RESEARCH NETWORK
罕见疾病临床研究网络脆性骨疾病联盟
- 批准号:
10392597 - 财政年份:2014
- 资助金额:
$ 0.28万 - 项目类别:
BRITTLE BONE DISORDERS CONSORTIUM OF THE RARE DISEASE CLINICAL RESEARCH NETWORK
罕见疾病临床研究网络脆性骨疾病联盟
- 批准号:
10515367 - 财政年份:2014
- 资助金额:
$ 0.28万 - 项目类别:
BRITTLE BONE DISORDERS CONSORTIUM OF THE RARE DISEASE CLINICAL RESEARCH NETWORK
罕见疾病临床研究网络脆性骨疾病联盟
- 批准号:
10267291 - 财政年份:2014
- 资助金额:
$ 0.28万 - 项目类别:














{{item.name}}会员




