Journal article

Hypertension and renin-angiotensin system blockers are not associated with expression of angiotensin-converting enzyme 2 (ACE2) in the kidney

Xiao Jiang, James M Eales, David Scannali, Alicja Nazgiewicz, Priscilla Prestes, Michelle Maier, Matthew Denniff, Xiaoguang Xu, Sushant Saluja, Eddie Cano-Gamez, Wojciech Wystrychowski, Monika Szulinska, Andrzej Antczak, Sean Byars, Damian Skrypnik, Maciej Glyda, Robert Krol, Joanna Zywiec, Ewa Zukowska-Szczechowska, Louise M Burrell Show all



AIMS: Angiotensin-converting enzyme 2 (ACE2) is the cellular entry point for severe acute respiratory syndrome coronavirus (SARS-CoV-2)-the cause of coronavirus disease 2019 (COVID-19). However, the effect of renin-angiotensin system (RAS)-inhibition on ACE2 expression in human tissues of key relevance to blood pressure regulation and COVID-19 infection has not previously been reported. METHODS AND RESULTS: We examined how hypertension, its major metabolic co-phenotypes, and antihypertensive medications relate to ACE2 renal expression using information from up to 436 patients whose kidney transcriptomes were characterized by RNA-sequencing. We further validated some of the key observations i..

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Awarded by British Heart Foundation

Awarded by Kidney Research UK

Awarded by Medical University of Silesia

Awarded by National Health and Medical Research project grant

Awarded by European Research Council

Awarded by British Heart Foundation Personal Chair

Awarded by ERA-CVD

Awarded by National Health and Medical Research Council Program

Awarded by Medical Research Future Fund

Awarded by Wellcome Trust

Awarded by Gates Cambridge Scholarship

Awarded by NIH

Funding Acknowledgements

This work was supported by British Heart Foundation project grants [PG/17/35/33001 and PG/19/16/34270] and Kidney Research UK [grant RP_017_20180302] to M.T., British Heart Foundation Personal Chair [CH/13/2/30154] and Manchester Academic Health Science Centre: Tissue Bank Grant to BK, Medical University of Silesia [grants KNW-1-152/N/7/K to J.Z. and KNW-1-171/N/6/K to W.W.]. F.C. and S.H. were supported by a National Health and Medical Research project grant [APP1104686]. T.J.G. was supported by the European Research Council [InflammaTENSION; ERC-CoG-726318], T.J.G. also acknowledges support from ERA-CVD [PLAQUEFIGHT/5/2018]. L.M.B. acknowledges support from National Health and Medical Research Council Program [Grant APP1055214] and Medical Research Future Fund [APP 1175865]. G.T. is supported by Open Targets and the Wellcome Trust [grant WT206194]. E.C.G. is supported by the Gates Cambridge Scholarship [OPP1144]. Access to TCGA kidneys and GTEx data has been granted by NIH [approvals 50804-2 and 50805-2]. The results published here are in part based upon data generated by the TCGA Research Network: thank the Oxford Genomics Centre at the Wellcome Centre for Human Genetics funded by Wellcome Trust [grant reference 203141/Z/16/Z] for the generation and initial processing of sequencing data.