Skip to main content

Philip Wenzel

Vascular Inflammation

Vascular inflammation leads to endothelial dysfunction and is an important contributing factor in the pathophysiology of cardiovascular diseases such as arterial hypertension and hypercholesterolemia. Importantly, vascular inflammation pathways have great potential in the development of new therapies: there are many potentially druggable targets that could benefit patients with myocardial infarction, venous thromboembolism and ischemia-reperfusion damage, as well as chronic inflammatory diseases such as psoriasis, and even stress and noise exposure.

In our group, we are particularly concerned with the importance of CD11b + myeloid cells, especially monocytes / macrophages. We are also interested in the influence of coagulation factors of the contact phase system, thrombin amplification and the tissue factor system in vascular inflammation.

Our research interests are:

  • Role of inflammatory myelomonocytic cells in vascular dysfunction and venous and arterial thrombosis

  • Proinflammatory cytokines and activation of inflammatory signaling pathways in vascular biology

  • Interplay of coagulation factors, leukocytes and platelets in vascular dysfunction and oxidative stress

Research website

Positions held

  • Since 2016: Deputy Director and Professor (W2) for Vascular Inflammation at the Center for Cardiology, Cardiology I, and Center for Thrombosis and Hemostasis (CTH), University Medical Center (UMC), Mainz
  • 2017: Principal Investigator, German Centre for Cardiovascular Research (DZHK)
  • 2011 - 2014: Junior Research Group Leader at the Centre for Thrombosis and Hemostasis (CTH), University Medical Center (UMC), Mainz 
  • 2003 - 2011: Residency in Internal Medicine and Cardiology, University Medical Center Hamburg Eppendorf; University Medical Center (UMC), Mainz


2010: Habilitation, University Medical Center (UMC), Mainz
2003: MD-Thesis, Institute for Sports Medicine, University Hamburg
1995 - 2002: Medical School, Friedrich Alexander-University, Erlangen-Nürnberg University Hamburg

Selected publications by Philip Wenzel

Molitor M, Rudi WS, Garlapati V, Finger S, Schuler R, Kossmann S, Lagrange J, Nguyen TS, Wild J, Knopp T, Karbach SH, Knorr M, Ruf W, Munzel T and Wenzel P (2021) Nox2+ myeloid cells drive vascular inflammation and endothelial dysfunction in heart failure after myocardial infarction via angiotensin II receptor type 1. Cardiovasc Res, 117:162–177 Link

Finger S, Knorr M, Molitor M, Schuler R, Garlapati V, Waisman A, Brandt M, Munzel T, Bopp T, Kossmann S, Karbach S and Wenzel P (2019) A sequential interferon gamma directed chemotactic cellular immune response determines survival and cardiac function post-myocardial infarction. Cardiovasc Res, 115:1907–1917 Link

Kossmann S*, Lagrange J*, Jackel S, Jurk K, Ehlken M, Schonfelder T, Weihert Y, Knorr M, Brandt M, Xia N, Li H, Daiber A, Oelze M, Reinhardt C, Lackner K, Gruber A, Monia B, Karbach SH, Walter U, Ruggeri ZM, Renne T, Ruf W, Münzel T and Wenzel P (2017) Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension. Sci Transl Med, 9:pii:eaah4923 (*indicates joint contribution) Link

Wenzel P, Rossmann H*, Muller C*, Kossmann S*, Oelze M, Schulz A, Arnold N, Simsek C, Lagrange J, Klemz R, Schonfelder T, Brandt M, Karbach SH, Knorr M, Finger S, Neukirch C, Hauser F, Beutel ME, Kroller-Schon S, Schulz E, Schnabel RB, Lackner K, Wild PS, Zeller T, Daiber A, Blankenberg S and Münzel T (2015) Heme oxygenase-1 suppresses a pro-inflammatory phenotype in monocytes and determines endothelial function and arterial hypertension in mice and humans. Eur Heart J, 36:3437–3446 (*indicates joint contribution) Link

Wenzel P*, Knorr M*, Kossmann S, Stratmann J, Hausding M, Schuhmacher S, Karbach SH, Schwenk M, Yogev N, Schulz E, Oelze M, Grabbe S, Jonuleit H, Becker C, Daiber A, Waisman A and Münzel T (2011) Lysozyme M-positive monocytes mediate angiotensin II-induced arterial hypertension and vascular dysfunction. Circulation, 124:1370–1381 (*indicates joint contribution) Link