Table 4.

Class IIB isoform-selective inhibitors for treatment of pulmonary fibrosis.

Study	Lung Fibrosis Model	HDAC Inhibition	Effect/Involved Molecules
Campiani et al. (2021) [174]	Organoid cultures derived from IPF basal cells, Ex vivo human lung model of fibrosis	“Compound 6h” HDAC6	Basal cell proliferation ↓ Bronchosphere formation ↓ Tubulin acetylation ↑ TGF-β dependent ECM synthesis ↓
Shan et al. (2008) [190]	TGF-β-stimulated A549 cells	Tubacin HDAC6 HDAC6 siRNA	Tubulin-hyperacetylation, restoration of E-cadherin, SMAD3 phosphorylation ↓ PAI1 ↓ COL1A1 ↓ inhibition of EMT
Deskin et al. (2016) [191]	TGF-β-stimulated A549 cells	Tubacin HDAC6 HDAC6 siRNA	Abrogation of TGF-β induced Notch1 signalling (HEY1, HES1 ↓) Acetylation of HSP90 (Ac-K294) p38 pathway ↓
Saito et al. (2017) [235]	TGF-β-stimulated human normal lung fibroblasts, Bleomycin mouse model	Tubastatin A HDAC6	In vitro and in vivo: Tubulin hyperacetylation, inhibition of PI3K-AKT pathway, FMD ↓ ECM ↓ amelioration of lung fibrosis

Definition of abbreviations: IPF: idiopathic pulmonary fibrosis; EMT: epithelial–mesenchymal transition; ECM: extracellular matrix; FMD: fibroblast-to-myofibroblast differentiation; siRNA: small interfering RNA; ↑: upregulation; ↓: downregulation.