PMC:7890668 / 6423-7583 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7890668","sourcedb":"PMC","sourceid":"7890668","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7890668","text":"We also uncovered an additional inference associating linagliptin and Angiotensin-Converting Enzyme II (ACE2), the host receptor for SARS-CoV-2 entry: Linagliptin-ACE2-T2D-COVID-19 (Fig. 1C). Downregulation of ACE2 expression in lung tissue has been associated with severe COVID-19 clinical outcomes (Nakhleh and Shehadeh, 2020). Expression of ACE2 is increased in patients with T2D; thus, ACE inhibitors and angiotensin-receptor blockers are commonly used to treat individuals with this condition (Pal and Bhansali, 2020). A recent study (Zhang et al., 2015) demonstrated that administration of linagliptin significantly upregulated ACE2 expression and was useful in preventing angiotensin II-induced cardiac fibrosis in animal models. It is yet unclear if upregulating ACE2 would be beneficial or detrimental to patients, especially those with T2D; nevertheless, this inference reveals an additional pathway linking linagliptin and COVID-19. Thus, COVID-KOP could help recovering known biochemical pathways associating a drug with COVID-19 (linagliptin-DPP4-T2D -COVID-19) as well as offer potentially novel inferences (linagliptin-TGFB1-Pneumonia-COVID-19).","tracks":[]}