亲爱的研友该休息了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

Fibrotic remodeling and tissue regeneration mechanisms define the therapeutic potential of human muscular progenitors

再生(生物学) 纤维化 祖细胞 旁分泌信号 伤口愈合 医学 祖细胞 细胞生物学 细胞外基质 干细胞 生物 病理 癌症研究 免疫学 内科学 受体
作者
Ya‐Chuan Hsiao,I‐Han Wang,Tsung‐Lin Yang
出处
期刊:Bioengineering & translational medicine [Wiley]
卷期号:8 (2)
标识
DOI:10.1002/btm2.10439
摘要

Fibrosis is an intrinsic biological reaction toward the challenges of tissue injury that is implicated in the wound-healing process. Although it is useful to efficiently mitigate the damage, progression of fibrosis is responsible for the morbidity and mortality occurring in a variety of diseases. Because of lacking effective treatments, there is an emerging need for exploring antifibrotic strategies. Cell therapy based on stem/progenitor cells is regarded as a promising approach for treating fibrotic diseases. Appropriate selection of cellular sources is required for beneficial results. Muscle precursor cells (MPCs) are specialized progenitors harvested from skeletal muscle for conducting muscle regeneration. Whether they are also effective in regulating fibrosis has seldom been explored and merits further investigation. MPCs were successfully harvested from all human samples regardless of demographic backgrounds. The extracellular matrices remodeling was enhanced through the paracrine effects mediated by MPCs. The suppression effects on fibrosis were confirmed in vivo when MPCs were transplanted into the diseased animals with oral submucous fibrosis. The data shown here revealed the potential of MPCs to be employed to simultaneously regulate both processes of fibrosis and tissue regeneration, supporting them as the promising cell candidates for development of the cell therapy for antifibrosis and tissue regeneration.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
科研通AI6.3应助LYCORIS采纳,获得10
8秒前
温柔的梦露完成签到,获得积分10
13秒前
28秒前
orixero应助ents采纳,获得30
33秒前
raita发布了新的文献求助30
33秒前
45秒前
科研通AI6.1应助默默的弼采纳,获得10
48秒前
raita完成签到,获得积分10
52秒前
wanci应助学者11111采纳,获得10
59秒前
1分钟前
1分钟前
Omni完成签到,获得积分10
1分钟前
paradox完成签到 ,获得积分10
1分钟前
科研通AI2S应助科研通管家采纳,获得10
1分钟前
1分钟前
1分钟前
1分钟前
NingJi应助Jack采纳,获得10
1分钟前
1分钟前
ZHH发布了新的文献求助10
1分钟前
可靠的雪碧完成签到,获得积分10
1分钟前
上官若男应助moonlin采纳,获得10
1分钟前
1分钟前
mlv完成签到,获得积分10
1分钟前
阳光的雪珊完成签到 ,获得积分10
1分钟前
2分钟前
2分钟前
ZHH完成签到,获得积分10
2分钟前
2分钟前
moonlin发布了新的文献求助10
2分钟前
LYCORIS发布了新的文献求助10
2分钟前
结实白云完成签到 ,获得积分10
2分钟前
2分钟前
txxxx发布了新的文献求助10
2分钟前
2分钟前
麻花阳完成签到,获得积分10
2分钟前
2分钟前
3分钟前
NingJi应助韩乐瑶采纳,获得10
3分钟前
3分钟前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Polymorphism and polytypism in crystals 1000
Social Cognition: Understanding People and Events 800
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6027829
求助须知:如何正确求助?哪些是违规求助? 7681418
关于积分的说明 16185776
捐赠科研通 5175202
什么是DOI,文献DOI怎么找? 2769294
邀请新用户注册赠送积分活动 1752705
关于科研通互助平台的介绍 1638483