To the editor
We read interesting correspondence reported by Liu et al. We would like to remind the forgotten aspects of ACE 2 enzyme.
ACE 2 enzyme doesn’t only hydrolyze angiotensin proteins, it also hydrolyzes ghrelin, Apelin-13 and other proteins. ARB and ACEI may increase ACE2 enzyme, which may increase the infection and decrease apelin-13 and ghrelin levels.
Ghrelin and Apelin-13 are reported to be neuroprotective.[3,4] Also, after ischemic injury, ghrelin seems to improve recovery. In COVID patients, taking these drugs may be more prone to stroke and other neurological complications. Decrease in ghrelin levels may increase the virus induced acute lung injury.5
Decreased level of these hormones may be responsible from several complications in COVID-19.
The other aspects of diseases and drugs that may effect ACE2 expression is they may also effect the response of drugs targetting COVID-19. We don’t know if vaccine efficiency may also be affected by these factors.
Liu M, Wang T, Zhou Y, Zhao Y, Zhang Y, Li J. Potential Role of ACE2 in Coronavirus Disease 2019 (COVID-19) Prevention and Management. J Transl Int Med 2020; 8: 9–19.
Vickers C, Hales P, Kaushik V, Dick L, Gavin J, Tang J et al. Hydrolysis of biological peptides by human angiotensin-converting enzyme-related carboxy-peptidase. J Biol Chem 2002; 277: 14838–43.
Bao H, Yang X, Huang Y, Qiu H, Huang G, Xiao H et al. The neuroprotective effect of apelin-13 in a mouse model of intracerebral hemorrhage. Neurosci Lett 2016; 628: 219–24.
Dong R, Chen M, Liu J, Kang J, Zhu S. Temporospatial effects of acyl-ghrelin on activation of astrocytes after ischaemic brain injury. J Neuroendocrinol 2019; 31: e12767.
Zheng H, Liang W, He W, Huang C, Chen Q, Yi H et al. Ghrelin attenuates sepsis-induced acute lung injury by inhibiting the NF-κB, iNOS, and Akt signaling in alveolar macrophages. Am J Physiol Lung Cell Mol Physiol 2019; 317: L381–91.
- Zitation exportieren
Zheng H, Liang W, He W, Huang C, Chen Q, Yi H)| false et al. Ghrelin attenuates sepsis-induced acute lung injury by inhibiting the NF-κB, iNOS, and Akt signaling in alveolar macrophages. Am J Physiol Lung Cell Mol Physiol 2019; 317: L381–91. 31242025 10.1152/ajplung.00253.2018