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GDF-11 as a Potential Cardiac Pro-Angiogenic Factor.

作者信息

Kato Tomohiro, Lee Richard T

机构信息

Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts, USA.

出版信息

JACC Basic Transl Sci. 2023 Jun 26;8(6):636-637. doi: 10.1016/j.jacbts.2023.04.003. eCollection 2023 Jun.

DOI:10.1016/j.jacbts.2023.04.003
PMID:37426538
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10322875/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f79/10322875/9d95402a3098/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f79/10322875/9d95402a3098/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f79/10322875/9d95402a3098/fx1.jpg

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本文引用的文献

1
Deficiency of GDF-11 Accelerates TAC-Induced Heart Failure by Impairing Cardiac Angiogenesis.生长分化因子11(GDF-11)缺乏通过损害心脏血管生成加速压力超负荷诱导的心力衰竭。
JACC Basic Transl Sci. 2023 Feb 22;8(6):617-635. doi: 10.1016/j.jacbts.2022.11.004. eCollection 2023 Jun.
2
Functional substitutions of amino acids that differ between GDF11 and GDF8 impact skeletal development and skeletal muscle.氨基酸在 GDF11 和 GDF8 之间的功能替换会影响骨骼发育和骨骼肌。
Life Sci Alliance. 2023 Jan 11;6(3). doi: 10.26508/lsa.202201662. Print 2023 Mar.
3
Heterozygous loss-of-function variants significantly expand the phenotypes associated with loss of GDF11.
杂合功能丧失变异显著扩展了与 GDF11 丧失相关的表型。
Genet Med. 2021 Oct;23(10):1889-1900. doi: 10.1038/s41436-021-01216-8. Epub 2021 Jun 10.
4
GDF11 Decreases Pressure Overload-Induced Hypertrophy, but Can Cause Severe Cachexia and Premature Death.GDF11 可减少压力超负荷引起的心肌肥厚,但可导致严重恶病质和过早死亡。
Circ Res. 2018 Nov 9;123(11):1220-1231. doi: 10.1161/CIRCRESAHA.118.312955.
5
Biochemistry and Biology of GDF11 and Myostatin: Similarities, Differences, and Questions for Future Investigation.生长分化因子11和肌肉生长抑制素的生物化学与生物学:异同点及未来研究问题
Circ Res. 2016 Apr 1;118(7):1125-41; discussion 1142. doi: 10.1161/CIRCRESAHA.116.308391.
6
Growth differentiation factor 11 is a circulating factor that reverses age-related cardiac hypertrophy.生长分化因子 11 是一种循环因子,可逆转与年龄相关的心肌肥厚。
Cell. 2013 May 9;153(4):828-39. doi: 10.1016/j.cell.2013.04.015.