Hacking mechanical memory

Hacking mechanical memory
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黑客机械记忆

DOI:
10.1016/j.bpj.2023.03.012
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发表时间:
2023
影响因子:
3.4
通讯作者:
Eyckmans, Jeroen
Eyckmans, Jeroen
中科院分区:
生物学3区
文献类型:
--
作者:
Eyckmans, Jeroen

文献摘要

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Autologous chondrocyte implantation (ACI) is a surgical procedure used to treat cartilage defects in articular joints. It involves removing healthy cartilage cells called chondrocytes from a patient, cultivating them in a laboratory for several weeks, and then reimplanting them into the patient’s joint to regenerate the damaged cartilage (1). Although ACI has been heralded as a promising technique for cartilage repair, expanding primary chondrocytes in conventional tissue culture vessels results in the irreversible loss of the chondrogenic phenotype and the emergence of a fibrotic one (2). This phenomenon, known as chondrocyte dedifferentiation, has hindered the clinical translation of ACI in patients. In this issue of Biophysical Journal, a study from Scott, Neu, and colleagues (3) provides new insights into how culturing chondrocytes on stiff substrates leads to changes in chromatin architecture and concomitant loss of the chondrocyte phenotype, which can be partially prevented by treatment with chromatin modifying inhibitors.