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Fig. 7 | Respiratory Research

Fig. 7

From: Inhibition of HDAC1 alleviates monocrotaline-induced pulmonary arterial remodeling through up-regulation of miR-34a

Fig. 7

Proposed mechanism for inhibition of histone deacetylases 1 (HDAC1) alleviating monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). Injection of MCT up-regulates HDAC1 expression, reduces miR-34a level, and subsequently increases the activity of matrix metalloproteinase 2/9 (MMP-2/9). The elevated activity of MMP-2/9 initiates degradation of extracellular matrix (ECM) and finally leads to excessive ECM accumulation through a vicious circle. In addition, tissue inhibitor of metalloproteinase 1/2 (TIMP-1/2) expression is also up-regulated to inhibit excessive MMP activity through a balancing mechanism. However, since the balancing effect is limited, the ratio of MMP-9/TIMP-1 and MMP-2/TIMP-2 is elevated. Inhibition of HDAC1 reverses the process in MCT-induced PAH through restoring miR-34a level

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Respiratory Research

ISSN: 1465-993X

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