Mission Statement

“Understanding the underlying mechanisms for better prevention and treatment of arterial hypertension and hypertension induced end-organ damage”

— Ulrich Wenzel, MD

Team Members

Post Doc

Marlies Bode, PhD

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MD student

Nicolas Ehnert

Technician

Stefan Gatzemeier

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Research

Increasing evidence indicates that hypertension and hypertensive end-organ damage are not only mediated by hemodynamic injury. Inflammation plays also an important role in the pathophysiology and contributes to the deleterious consequences of arterial hypertension. Sodium intake is indispensable for normal body function but can be detrimental when taken in excess of dietary requirements. Recent data show that sodium levels also modulate the function of monocyte/macrophages, dendritic cells, and different T cell subsets. Some of these effects are mediated by changes in the microbiome and metabolome that can be found after high salt intake.

The purpose of our work is to discover the mechanisms underlying arterial hypertension to better understand arterial hypertension and the resulting end-organ damage. We focus on three points:

  1. Role of the complement system in hypertension.
  2. Role of aldosterone and the mineralocorticoid receptor in inflammatory cells.
  3. Pathogenesis of so-called malignant hypertension and malignant nephrosclerosis in humans.

Figure 1: Our current concept explaining arterial hypertension (from Hengel et al. 2022). We call it a modified mosaic theory putting inflammation and salt in the center.

Figure 2: Proinflamamtory effects of the mineralocorticoid receptor in innate and adapive immune cells (from Hengel et al 2022). Recent data suggest that the mineralocorticoid receptor is expressed in inflammatory cells and has proinflammatory effects.

Figure 3: The pathogensis of renal injury in so called malignannt nephrosclerosis is not understood. It is a form of thrombotic microangiopathy defined by progressive narrowing of interlobular arterial branches and afferent arterioles with intima fibrosis and onion-like appearance of intimal scarring as shown below (histology provided by T. Wiech).

©Ulrich Wenzel

CV

Current Position

Senior Physician

University Training
1983 - 1989

Medical School, Freie Universität Berlin, Germany

Academic qualifications
2002 - 2020

Habilitation and Venia legendi Internal Medicine, University Medical Center Hamburg Eppendorf, UKE

1992

Medical Thesis, Freie Universität Berlin

Previous professional career

Clinical postgraduate education:

2005

Hypertensiologe DHL®

2004

Board Certification Nephrology

2000

Board Certification Internal Medicine

Scientific postgraduate education:

1993 - 1995

Post-Doc, University of Texas, Health Science Center at San Antonio, Department of Medicine, Division of Nephrology (H. Abboud, M. D., Professor of Medicine), San Antonio, Texas, USA

Selected awards and honors
2020 - 2023 - 2020

President German Society of Hypertension

2016

Franz Gross Award, Germany Society of Hypertension

2003

Dr. Martini-Award, Hamburg, Germany

2001

Adalbert Buding Award, Germany Society of Hypertension

1988 - 1989

Fellow Studienstiftung des Deutschen Volkes

Selected publications

1.

The role of the mineralocorticoid receptor in immune cells in cardiovascular disease.
van der Heijden CDCC, Bode M, Riksen NP, Wenzel UO. Br J Pharmacol. 179:3135-3151, 2022.

2.

Mosaic theory revisited: inflammation and salt play a central role in arterial hypertension.
Hengel F, Benitah JP, Wenzel UO. Cell Mol Immunol. 19:561-576, 2022.

3.

The role of complement in arterial hypertension and hypertensive end organ damage..
Wenzel UO, Kemper C, Bode M. Br J Pharmacol. 178:2849-2862, 2021.

4.

Immune mechanisms in arterial hypertension. Recent advances.
Wenzel UO, Ehmke H, Bode M. Cell Tissue Res. 385:393-404, 2021.

5.

B6.Rag1 Knockout Mice Generated at the Jackson Laboratory in 2009 Show a Robust Wild-Type Hypertensive Phenotype in Response to Ang II (Angiotensin II).
Seniuk A, Thiele JL, Stubbe A, Oser P, Rosendahl A, Bode M, Meyer-Schwesinger C, Wenzel UO, Ehmke H. Hypertension. 75:1110-1116, 2020.

6.

The chemokine receptor CX3CR1 reduces renal injury in mice with angiotensin II-induced hypertension.
Ahadzadeh E, Rosendahl A, Czesla D, Steffens P, Prüßner L, Meyer-Schwesinger C, Wanner N, Paust HJ, Huber TB, Stahl RAK, Wiech T, Kurts C, Seniuk A, Ehmke H, Wenzel UO. Am J Physiol Renal Physiol. 315:F1526-F1535, 2018.

7.

Adaptive immunity and IL-17A in chronic kidney disease in mice.
Rosendahl A, Kabiri R, Bode M, Klinge S, Ehmke H, Mittrücker HW, Wenzel UO. Brit J Pharmacol. 176:2002-2014, 2019.

8.

Salt, inflammation, IL-17 and hypertension.
Wenzel UO, Bode M, Kurts C, Ehmke H. Br J Pharmacol. 176:1853-1863, 2019.

9.

The complement receptor C5aR1 contributes to renal damage but protects the heart in angiotensin II-induced hypertension.
Weiss S, Rosendahl A, Czesla D, Meyer-Schwesinger C, Stahl R, Ehmke H, Kurts C, Zipfel P, Köhl J, Wenzel UO. Am J Physiol Renal Physiol. 310:F1356-65, 2016.

10.

Immune Mechanisms in Arterial Hypertension.
Wenzel UO, Turner JE, Krebs C, Kurts C, Harrison DG, Ehmke H. J Am Soc Nephrol. 27:677-86, 2016.

Funding

Martinistraße 52
Campus Research N27
20246 Hamburg Germany
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University Medical Center Hamburg - Eppendorf