Figure 3

Overview of processes affected by HDAC inhibition in liver and kidney fibrosis. In experimental models of both liver and kidney fibrosis the beneficial effects of HDAC inhibitors have been reported as discussed in this review. (A) Specifically for liver, most studies have focused on the effects on stellate cell activation. Different aspects of this process have been described, such as, for example, the effects on matrix remodeling proteins. By inhibiting HSC activation, the development of fibrosis can be inhibited. (B) In kidneys, the favorable properties of HDAC inhibitors can be found in both the glomerular and tubulointerstitial compartment, where processes, such as proliferation, apoptosis, ECM deposition and inflammation, are hampered. Abrogating the pathological processes of glomerulosclerosis and tubulointerstitial (TI) fibrosis can potentially inhibit the development and progression of chronic kidney disease (CKD).