HDAC6 and pulmonary fibrosis: Therefore, it is plausible that loss of HDAC6’s ubiquitin-binding function aggravates pulmonary fibrosis by causing defective autophagy (as a result of deregulated aggresome formation) and/or activation of NLRP3 inflammasome [43, 44], whereas loss or inhibition of HDAC6’s deacetylating function ameliorates pulmonary fibrosis by hyperacetylating target proteins.