High-selective HDAC6 inhibitor alleviates bone marrow fibrosis through inhibiting collagen formation and extracellular matrix deposition.

ABSTRACT: Bone marrow fibrosis (BMF) impairs normal hematopoietic functions in patients. The overactivation of the TGF-β signaling pathway is regarded as one of the offenders causing disease progression. Thus, factors capable of regulating TGF-β secretion hold great potential in reversing fibrotic diseases. One such factor is histone deacetylase inhibitors (HDACis), which can modulate the expression of TGF-β. Our previous study successfully synthesized a selective HDAC6 inhibitor, J22352, for pulmonary fibrosis; however, the treatment efficacies on BMF remain unclear. Therefore, in this study, we treated bone marrow-derived myofibroblasts with J22352. The results showed that J22352 significantly reduced cell viability, induced apoptosis, and inhibited extracellular matrix (ECM) accumulation. Liquid

SUBMITTER: Ke CH 

PROVIDER: S-EPMC12317122 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature