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Cardiovascular Therapeutics
Cardiovascular Therapeutics

Targeting cardiovascular and age-associated diseases

Scientific focus

Many organs harbor resident stem cells that enable tissue-specific regeneration throughout adulthood. Our research, along with others, has shown that cellular fate decisions are not irreversible but can be reverted and reprogrammed to an extent that differentiated cells acquire stem cell like features.

The Cardiovascular Therapeutics team, headed by Dr. Johnny Kim and Dr. Boris Strilic employs systems biology approaches, advanced in-vitro models, and tissue-specific knockout mice to investigate the molecular mechanisms of cell fate decisions and their reversion. By deciphering these molecular principles, our interdisciplinary team aims to leverage this knowledge to combat the course of diseases such as cardiovascular diseases and cancer, as well as the decline in regenerative potential with aging. A key aspect of our research is thus based on controlled reactivation of early developmental programs to initiate epigenetic rejuvenation and restore or synthesize regenerative potential.

Our overarching goal is to develop novel therapeutic strategies against cardiovascular and age-associated diseases.

Selected collaborations

curATime – Cluster for Atherothrombosis and Individualized medicine is our BMBF-funded "Cluster4Future", which we initiated with the University Medical Center Mainz, the German Research Center for Artificial Intelligence (DFKI) and many more partners from academia and industry. Within curATime, we use artificial intelligence to identify disease-relevant factors that link to causes of atherothrombosis. We want to identify molecularly defined precision interventions and hope that we will be able to reduce incidence, impact and mortality of cardiovascular diseases.

One of the lighthouse projects is curAIntervent - Locoregional RNA immunotherapy of atherothrombosis, led by Dr. Johnny Kim. Within this project, the preclinical foundation for RNA-based therapy options against atherothrombosis will be developed. Read more about the Project curAIntervent here.

 

Recently, we also started a cooperation with the renowed Yale University that is focusing on age-associated cardiovascular diseases.

Contact

+49 (0) 6131 2161-600 (Johnny Kim)
+49 (0) 6131 2161-601 (Boris Strilic)

therapeutic-cardiology@tron-mainz.de

Selected publications of team members

Zhu Y, Ackers-Johnson M, Shanmugam MK, Pakkiri LS, Drum CL, Chen Y, Kim J, Paltzer WG, Mahmoud AI, Tan WLW, Lee MCJ, Jiang J, Luu DAT,
Ng SL, Li PYQ, Wang A, Qi R, Ong GJX, Ng TY, Haigh JJ, Tiang Z, Richards AM, Foo RSY.  
Asparagine Synthetase Marks a Distinct Dependency Threshold for Cardiomyocyte Dedifferentiation. 
Circulation 2024
DOI

Vega-Sendino M, Lüttmann F, T Olbrich T, Yanpu Chen Y, Kuenne C, Stein P, Tillo D, Carey G, Zhong J, Savy V, Radonova L, Lu T, Saykali B, Kim K,
Domingo C, Schüler L, Günther S, Bentsen M, Bosnakovski D, Schöler H, Kyba M, Maity T, Jenkins L, Looso M, Williams C, Kim J, Ruiz S. 
The homeobox transcription factor DUXBL controls exit from totipotency 
Nat Genet 2024 
DOI

Li R, Shao J, Jin YJ, Kawase H, Ong YT, Troidl K, Quan Q, Wang L, Bonnavion R, Wietelmann A, Helmbacher F, Potente M,
Graumann J, Wettschureck N, Offermanns S. 
Endothelial FAT1 inhibits angiogenesis by controlling YAP/TAZ protein degradation via E3 ligase MIB2. 
Nat Commun. 2023 
DOI

Stüdemann T, Rössinger J, Manthey C, Geertz B, Srikantharajah R, von Bibra C, Shibamiya A, Köhne M, Wiehler A,
Wiegert JS, Eschenhagen T, Weinberger F.  
Contractile Force of Transplanted Cardiomyocytes Actively Supports Heart Function After Injury. 
Circulation 2022 
DOI

Chen Y, Lüttmann FF, Schoger E, Schöler HR, Zelarayán LC, Kim KP, Haigh JJ, Kim J, Braun T.
Reversible reprogramming of cardiomyocytes to a fetal state drives heart regeneration in mice.  
Science 2021
DOI

Kim KP, Choi J, Yoon J, Bruder JM, Shin B, Kim J, Arauzo-Bravo MJ, Han D, Wu G, Han DW, Kim J, Cramer P, Schöler HR.
Permissive epigenomes endow reprogramming competence to transcriptional regulators.
Nat Chem Biol 2021
DOI

Preussner J, Zhong J, Sreenivasan K, Günther S, Engleitner T, Künne C, Glatzel M, Rad R, Looso M, Braun T, Kim J.
Oncogenic Amplification of Zygotic Dux Factors in Regenerating p53-Deficient Muscle Stem Cells Defines a Molecular Cancer Subtype.
Cell Stem Cell 2018
DOI 

Strilic B, Yang L, Albarrán-Juárez J, Wachsmuth L, Han K, Müller UC, Pasparakis M, Offermanns S.
Tumour-cell-induced endothelial cell necroptosis via death receptor 6 promotes metastasis.
Nature  2016
DOI