Our research focus
Mechanisms of cardiovascular calcification
Cardiovascular calcification, which is defined as the pathological calcification of heart valves and arteries, has emerged as a predictor of and contributor to cardiovascular morbidity and mortality. While the association between cardiovascular calcification and cardiovascular events has been established clinically, the molecular mechanisms that control vascular calcification are not well understood. Our research has considerable clinical interest and is an important contribution in advancing our understanding of cardiovascular calcification, particularly in patients with renal failure who have accelerated arterial and valvular calcification. Moreover, emerging evidence suggests that microcalcification may contribute to plaque rupture the leading cause of myocardial infarction.
Our major area of research is the identification of differential mechanisms for cardiovascular calcification and bone remodeling to detect novel therapeutic targets for vascular calcification, which do not negatively impact bone mineralization.
PD Dr. rer. nat. Claudia Goettsch, PhD
Department of Internal Medicine I - Cardiology
Uniklinik RWTH Aachen
Phone: +49 241 80-37312
Phone: +49 241-80 80378
Stefan Reinhold, M.Sc.
Visiting scientist, PhD Student
European Union’s Horizon 2020 ITN INTRICARE
We are continuously looking for talented MD and PhD students with an interest in cardiovascular biology. If you are interested please send your CV and a letter of intent to Dr. Goettsch: cgoettschukaachende
For a complete reference list please see PubMed* Link
Kaesler N, Goettsch C, Weis D, Schurgers L, Hellmann B, Floege J, Kramann R. Magnesium but not nicotinamide prevents vascular calcification in experimental uraemia. Nephrol Dial Transplant. 2019.
Wendt S, Goetzenich A, Goettsch C, Stoppe C, Bleilevens C, Kraemer S, Benstoem C. Evaluation of the cardioprotective potential of extracellular vesicles - a systematic review and meta-analysis. Sci Rep. 2018;8:15702.
Goettsch C, Iwata H, Hutcheson JD, O'Donnell CJ, Chapurlat R, Cook NR, Aikawa M, Szulc P, Aikawa E. Serum Sortilin Associates With Aortic Calcification and Cardiovascular Risk in Men. Arterioscler Thromb Vasc Biol 2017;37:1005-1011.
Kramann R, Goettsch C, Wongboonsin J, Iwata H, Schneider RK, Kuppe C, Kaesler N, Chang-Panesso M, Machado F, Gratwohl S, Vemuri C, Madhurima K, Hutcheson JD, Jain S, Aikawa E, Humphreys EB. Adventitial MSC-like cells are progenitors of vascular smooth muscle cells and drive vascular calcification in chronic kidney disease. Cell Stem Cell 2016;19:628-642.
Iwata H, Goettsch C, Sharma A, Ricchiuto P, Goh WWB, Halu A, Yamada I, Yoshida H, Hara T, Wei M, Inoue N, Fukuda D, Mojcher A, Mattson PC, Barabasi AL, Boothby N, Aikawa E, Singh SA, Aikawa M. PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP ribosylation. Nat Commun 2016; 7:12849.
Goettsch C, Hutcheson JD, Hagita S, Rogers M, Pham TH, Creager MD, Jung C, Mlynarchik AK, Kjolby, MF, Aikawa M, Aikawa E. Induction of cardiovascular calcification in non-transgenic mice via a single injection of PCSK9 adeno-associated viral vector. Atherosclerosis 2016;215:109-118.
Goettsch C, Hutcheson JD, Aikawa M, Iwata H, Pham T, Nykjaer A, Kjolby M, Rogers M, Michel T, Shibasaki M, Hagita S, Kramann R, Rader DJ, Libby P, Singh SA, Aikawa E. Sortilin mediates vascular calcification via its recruitment into extracellular vesicles. J Clin Invest 2016; 126:1323-36.
Hutcheson JD, Goettsch C, Bertazzo S, Maldonado N, Ruiz JL, Goh WWB, Yabusaki K, Faits T, Bouten C, Franck G, Quillard T, Libby P, Aikawa M, Weinbaum S, Aikawa E. Genesis and growth of extracellular-vesicle-derived microcalcification in atherosclerotic plaques. Nat Mater 2016;15:335-43.
Goettsch C, Babelova A, Trummer O, Erben RE, Rauner M, Rammelt S, Weissmann N, Weinberger V, Benkhoff S, Kampschulte M, Obermayer-Pietsch B, Hofbauer LC, Brandes RP, Schröder K. NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis. J Clin Invest 2013;123:4731-38.
New SE, Goettsch C, Aikawa M, Marchini JF, Shibasaki M, Yabusaki K, Libby P, Shanahan CM, Croce K, Aikawa, E. Macrophage-Derived Matrix Vesicles: An Alternative Novel Mechanism for Microcalcification in Atherosclerotic Plaques. Circ Res 2013;113:72-7.
Goettsch C, Kliemt S, Sinningen K, von Bergen M, Hofbauer LC, Kalkhof S. Quantitative proteomics reveals novel functions of osteoclast-associated receptor in STAT signaling and cell adhesion in human endothelial cells. J Mol Cell Cardiol 2012;53:829-837.
Goettsch C, Rauner M, Sinningen K, Helas S, Al-Fakhri N, Nemeth K, Hamann C, Kopprasch S, Aikawa E, Bornstein SR, Schoppet M, Hofbauer LC. The osteoclast-associated receptor (OSCAR) is a novel receptor regulated by oxidized low density lipoprotein in human endothelial cells. Endocrinology 2011;152:4915-26.
Goettsch C, Rauner M, Pacyna N, Hempel U, Bornstein SR, Hofbauer LC. MiR-125b regulates vascular smooth muscle cell calcification. Am J Pathol 2011;179:1594-600.
Goettsch C, Rauner M, Hamann C, Hempel U, Bornstein SR, Hofbauer LC. Nuclear factor of activated T cells is involved in oxidized low-density lipoprotein-induced osteogenic transdifferentiation of vascular smooth muscle cells. Diabetologia 2011;54:2690-701.
Goettsch C, Goettsch W, Brux M, Haschke C, Brunssen C, Muller G, Bornstein SR, Duerrschmidt N, Wagner AH, Morawietz H. Arterial flow reduces oxidative stress via an antioxidant response element and Oct-1 binding site within the NADPH oxidase 4 promoter in endothelial cells. Basic Res Cardiol 2011;106:551-561.
- German Research Fundation (DFG)
- Sonderforschungsbereich Transregio SFB219 - German Research Fundation (DFG)
- ERA-CVD (Federal Ministry of Education and Research, BMBF)
- European Union’s Horizon 2020 ITN INTRICARE
- Internal funding (START)
Carina Ciliox, medical student in our group, receives one of the precious Otto-Hess scholarshipsfrom the German Cardiac Society. The scholarship provides financial support for medical students to perform an experimental medical doctoral thesis for one year. Carina will study the role of cytoskeletal reorganization in cardiovascular calcification.