Dipeptidyl peptidase 3, a marker of the antagonist pathway of the renin–angiotensin–aldosterone system in patients with heart failure-Reference-Cited by-同舟云学术

Dipeptidyl peptidase 3, a marker of the antagonist pathway of the renin–angiotensin–aldosterone system in patients with heart failure

Published:2021-03-30 Issue:6 Volume:23 Page:947-953
ISSN:1388-9842
Container-title:European Journal of Heart Failure
language:en
Short-container-title:Eur J Heart Fail

Author:

Boorsma Eva M.¹,Maaten Jozine M.¹,Damman Kevin¹,Veldhuisen Dirk J.¹,Dickstein Kenneth²³,Anker Stefan D.⁴⁵,Filippatos Gerasimos⁶,Lang Chim C.⁷,Metra Marco⁸,Santos Karine⁹,Voors Adriaan A.¹

Affiliation:

1. University of Groningen, University Medical Center Groningen Groningen The Netherlands

2. University of Bergen Bergen Norway

3. Stavanger University Hospital Stavanger Norway

4. Department of Cardiology (CVK); and Berlin Institute of Health Center for Regenerative Therapies (BCRT); German Centre for Cardiovascular Research (DZHK) partner site Berlin, Charité Universitätsmedizin Berlin Berlin Germany

5. Department of Cardiology and Pneumology University Medical Center Göttingen, Georg‐August University Göttingen Germany

6. National and Kapodistrian University of Athens, School of Medicine, Department of Cardiology, Heart Failure Unit Athens University Hospital Attikon Athens Greece

7. Division of Molecular & Clinical Medicine University of Dundee Dundee UK

8. Institute of Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health University of Brescia Brescia Italy

9. 4TEEN4 Pharmaceuticals GmbH Hennigsdorf Germany

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ejhf.2158

Reference22 articles.

1. Identification of dipeptidyl peptidase 3 as the Angiotensin-(1–7) degrading peptidase in human HK-2 renal epithelial cells

2. Novel Therapeutic Role for Dipeptidyl Peptidase III in the Treatment of Hypertension

3. ACE2, angiotensin-(1-7) and Mas receptor axis in inflammation and fibrosis

4. Angiotensin-(1-7) Blockade Attenuates Captopril- or Hydralazine-induced Cardiovascular Protection in Spontaneously Hypertensive Rats Treated With NG-nitro-l-Arginine Methyl Ester

5. Azilsartan Is Associated With Increased Circulating Angiotensin-(1-7) Levels and Reduced Renovascular 20-HETE Levels

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