Mammalian organ regeneration in spiny mice.

IF 1.7 3区 生物学 Q4 CELL BIOLOGY
Daryl M Okamura, Elizabeth D Nguyen, Sarah J Collins, Kevin Yoon, Joshua B Gere, Mary C M Weiser-Evans, David R Beier, Mark W Majesky
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引用次数: 0

Abstract

Fibrosis-driven solid organ failure is a major world-wide health burden with few therapeutic options. Spiny mice (genus: Acomys) are terrestrial mammals that regenerate severe skin wounds without fibrotic scars to evade predators. Recent studies have shown that spiny mice also regenerate acute ischemic and traumatic injuries to kidney, heart, spinal cord, and skeletal muscle. A common feature of this evolved wound healing response is a lack of formation of fibrotic scar tissue that degrades organ function, inhibits regeneration, and leads to organ failure. Complex tissue regeneration is an extremely rare property among mammalian species. In this article, we discuss the evidence that Acomys represents an emerging model organism that offers a unique opportunity for the biomedical community to investigate and clinically translate molecular mechanisms of scarless wound healing and regeneration of organ function in a mammalian species.

Abstract Image

棘皮小鼠的哺乳动物器官再生
纤维化导致的实体器官衰竭是世界范围内的主要健康负担,但治疗方法却很少。刺鼠(属:Acomys)是一种陆生哺乳动物,能使严重的皮肤伤口再生,而不留下纤维化疤痕,以躲避捕食者。最近的研究表明,刺鼠还能使肾脏、心脏、脊髓和骨骼肌的急性缺血性和创伤性损伤再生。这种进化的伤口愈合反应的共同特征是不形成纤维化疤痕组织,而纤维化疤痕组织会降低器官功能、抑制再生并导致器官衰竭。复杂的组织再生是哺乳动物中极为罕见的特性。在这篇文章中,我们讨论了 Acomys 代表一种新兴模式生物的证据,这种模式生物为生物医学界研究和临床转化哺乳动物物种无疤痕伤口愈合和器官功能再生的分子机制提供了一个独特的机会。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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