ACE/ACE2 Ratio and MMP-9 Activity as Potential Biomarkers in Tuberculous Pleural Effusions

Hsieh, Wen-Yeh; Kuan, Tang-Ching; Cheng, Kun-Shan; Liao, Yan-Chiou; Chen, Mu-Yuan; Lin, Pei-Heng; Hsu, Yuan-Chang; Huang, Chen-Yi; Hsu, Wei-Hua; Yu, Sheng-Yao; Lin, Chih-Sheng

ACE2, a close homologue of ACE, functions as a negative regulator of the angiotensin system and was identified as a key receptor for severe acute respiratory syndrome coronavirus infections [5, 6] . ACE2 reduces the generation of Ang II by catalysing the conversion of Ang I to Ang1-9 and facilitating hydrolysis of Ang II to Ang1-7. Ang1-7 has been recognised as a potential endogenous inhibitor of the classical RAS cascade [7] . Hence, the ACE2Ang1-7 axis may be an important negative modulator of Ang II bioactivity, counteracting the effects of ACE in determining net tissue Ang II levels. Abnormally elevated ACE combined with decreased ACE2 expression may be involved in fibrotic processes in vitro and in vivo, and the mechanism may involve expression and activation of specific MMPs [8] . Recently, abnormal pleural MMP levels, e.g., MMP-2 and MMP-9, have been reported, and the association between MMPs and development of pleurisy has been investigated [9, 10, 11] .