Tubastatin ameliorates pulmonary fibrosis by targeting the TGFβ-PI3K-Akt pathway.
Shigeki SaitoYan ZhuangBin ShanSvitlana DanchukFayong LuoMartina KorfeiAndreas GuentherJoseph A LaskyPublished in: PloS one (2017)
HDAC6 expression is altered during lung fibrogenesis. Tubastatin represses TGF-β1-induced collagen expression, by diminishing Akt phosphorylation and regulating downstream targets such as HIF-1α-VEGF axis and autophagy. Tubastatin-treated WT mice are protected against bleomycin-induced fibrosis, but HDAC6 KO mice are not. Our data suggest that Tubastatin ameliorates pulmonary fibrosis, by targeting the TGFβ-PI3K-Akt pathway, likely via an HDAC6-independent mechanism.
Keyphrases
- pulmonary fibrosis
- transforming growth factor
- poor prognosis
- high glucose
- endothelial cells
- histone deacetylase
- signaling pathway
- high fat diet induced
- cell death
- cell proliferation
- vascular endothelial growth factor
- adipose tissue
- endoplasmic reticulum stress
- machine learning
- big data
- long non coding rna
- insulin resistance
- artificial intelligence
- wound healing
- deep learning