Ljubica Matic

Ljubica Matic

Principal Researcher | Docent

Molecular biologist dedicated to developing new drug targets and biomarkers for vascular disease

Telephone: +46852482726
Visiting address: Karolinska Institutet, BioClinicum J8:20, Visionsgatan 4, 17164 Solna
Postal address: K1 Molekylär medicin och kirurgi, K1 MMK Kärlkirurgi, 171 76 Stockholm

About me

  • Ljubica Matic is Assoc Prof of Molecular Medicine and Principal Researcher in the Vascular Surgery Division at Karolinska Institute. She obtained her MSc degree in Molecular Biology from Belgrade University, Serbia and a PhD in Medical Biochemistry from Karolinska Institute in 2012. Since 2019 she is Group Leader for Translational Vascular Medicine at the Center for Molecular Medicine, KI dedicated to translational research on novel therapeutic and diagnostic targets for the management of cardiovascular disease, specifically atherosclerosis and restenosis complications.

    Her work has over the years been distinguished with grants and awards from the Swedish Research Council, Swedish Heart-Lung Foundation, Swedish Society for Medical Research, KI Faculty Consolidator grant, American Heart Association (Daniel Steinberg Early Career Investigator award in 2023) and the Royal Swedish Academy of Sciences (Sven and Ebba Hagberg Award in 2019). She is the KI Principal Investigator for several ongoing EU Horizon projects, as well as the Leducq network of excellence ATHENA, and La Caixa project AtheroPTM. 

    Ljubica Matic works as expert reviewer for the Swedish Research Council, Swedish Heart-Lung Foundation, European Research Council, British and Dutch Heart Foundations, Danish Cardiovascular Academy, etc. She is elected Fellow of the European Society of Cardiology (FESC), Steering Board Member for the KI Research Incubator (KIRI), member of the Women’s Leadership Committee in the International Society of Applied Cardiovascular Biomedicine, and Management Committee member for the EU COST actions AtheroNET and CardioPharmaGENET.

    Her editorial work includes positions as Editorial Board member for the Vascular Pharmacology journal, and Associated Editor of the Atheroclerosis journal. She has >110 publications with over 5500 citations and h-index 46. 

Research

  • Matic group (https://linktr.ee/ljubicamatic) utilizes innovative, integrated in silico pipelines for exploration of the Biobank of Karolinska Endarterectomy (BiKE, est 2002), Biobank of Karolinska lower limb Peripheral Arterial Disease (BiKPAD, est 2025) and Biobank of Karolinska Smooth Muscle Cells (BiKSMC, est 2024), to identify smooth muscle cell related targets that stand in direct causal relationship with human vascular disease. Target discovery via AI/ML guided multi-modal data integrations, is followed by phenotyping, challenge and proof-of-concept interventional studies in murine vascular injury and disease models, as well as in vitro investigations using primary human smooth muscle cells. 

    With this multi-disciplinary approach, the mission of Ljubica Matic is to create a powerful platform for extrapolation of basic research results into the various realms of clinical cardiovascular disease. To this end, she collaborates with Big Pharma and is a co-inventor of totally 21 patents, accelerating the developments from target discovery to patient treatments. 

Teaching

  • Since 2004, Ljubica Matic has continuously devoted 20% of her time to pedagogical work as a lecturer, supervisor and course leader for PhD students in the Cardiovascular Program and undergraduate students in the Medicine and Biomedicine Programs at KI. Since 2013 she has been Director for the PhD course in Vascular Cell Biology, Cardiovascular Program, KI. Since 2021 she acts as Assoc Director for the KI MSc Global Biomedicine program, elective track in Circulation, Metabolism and Endocrinology. 

    Over the years, she has also organised free-standing international PhD courses in cardiovascular disease in the framework of the EU Horizon Marie Sklodowska Curie ITN projects, EU ERASMUS program, as well as courses in gold standard biobanking practices for the EU Widera program. 

Articles

All other publications

Grants

  • Swedish Heart-Lung Foundation
    1 January 2026 - 31 December 2027
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and their druggability evaluated via proof-of-concept in vivo models in mice. Significance: With this translational approach, the project is poised to push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • Swedish Heart-Lung Foundation
    1 January 2025 - 31 December 2027
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. Finally, we will test complementation of current therapies with SMC-targeted plaque stabilisation in small and large animal models, to alleviate total disease burden. Significance: With this translational approach, the project will push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • European Commission
    1 October 2024 - 30 September 2027
    There are over 330 million people living on the planet affected by one of over 6,000 identified genetic rare diseases (RD). They urgently need timely diagnosis and development of specific treatments. Although Europe leads the way in RD research, there is a clear gap in research and innovation (R&I) between countries. To bridge this gap, networking and knowledge sharing between IMGGE (Institute of Molecular Genetics and Genetic Engineering, Serbia) and 3 world-class counterparts at EU level - KI (Karolinska Institute, Sweden), CNAG (National Center for Genomic Analysis, Spain) and UAM (Autonomous University of Madrid, Spain) is envisioned. BRIDGING-RD’s objectives are: (1) upgrade the IMGGE RD Biobank to reach full interoperability of genetic and phenotypic data in order to increase participation in transnational research and innovation projects related to human health
    (2) upgrade bioinformatics pipelines specific to RD to increase the rate of solved RD cases in IMGGE’s RD Biobank
    (3) upgrade capacity for modelling of metabolic diseases as well as capacity to test small molecule drugs, in order to increase the number of translational studies
    (4) upgrade research support offices in order to increase success in obtaining funds from research and/or innovation agencies, industry, foundations etc. Objectives will be achieved through staff exchanges, expert visits, trainings or workshops, conference attendance, joint summer schools and dissemination/outreach activities. Crucially, an exploratory R&I project, engaging all partners will focus on identifying an innovative drug, pharmacochaperone, for a selected metabolic RD. BRIDGING-RD will have impact by significantly improving the scientific excellence and innovation capacity of IMGGE, raising its research reputation and research management skills. It will also impact networking and mobility of qualified scientists in the RD field, thus boosting creativity and ultimately enhancing economic growth at the European level.
  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Our hypothesis is that exploration of pathways controlling SMC subphenotypes can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the best available treatments. We will develop in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. We will test complementation of current therapies with SMC-targeted plaque stabilisation, to alleviate total disease burden.With this translational approach, the project will push the knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in treatment of complex CVD.
  • European Commission
    1 January 2024 - 31 December 2027
    Healthcare is the fasted growing EU27 expenditure. Personalised medicine, comprising tailored approaches for prevention, diagnosis, monitoring and treatment is essential to reduce the burden of disease and improve the quality of life. Integration of multiple data types (multimodal data) into artificial intelligence models is required for the development of accurate and personalised interventions. This is particularly true for the inclusion of genomic data, which is information-rich and individual-specific, and more routinely available as the cost of sequencing continues to fall. Multimodal data integration is complex due to privacy & governance requirements, the presence of multiple standards, distinct data formats, and underlying data complexity and volume. NextGen tools will remove barriers in data integration several cardiovascular use cases. NextGen deliverables will include tooling for multimodal data integration and research portability, extension of secure federated analytics to genomic computation, more effective federated learning over distributed infrastructures, more effective and accessible tools for genomic data analysis
    improved clinical efficiency of variant prioritisation
    scalable genomic data curation
    and improved data discoverability and data management. A comprehensive gap analysis of the existing landscape, factoring ongoing initiatives will ensure NextGen deliverables are forward-looking and complementary. NextGen embedded governance framework and robust regulatory processes will ensure secure multi-jurisdictional multiomic multimodal data access aligned with initiatives including “1+ Million Genomes” and the European Health Data Space. Several real-world pilots will demonstrate the effectiveness of NextGen tools and will be integrated in the NextGen Pathfinder network of five collaborating clinical sites as a self-contained data ecosystem and comprehensive proof of concept.
  • Swedish Heart-Lung Foundation
    1 January 2024 - 31 December 2026
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. Finally, we will test complementation of current therapies with SMC-targeted plaque stabilisation in small and large animal models, to alleviate total disease burden. Significance: With this translational approach, the project will push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • Swedish Research Council
    1 January 2022 - 31 December 2025
  • Swedish Heart-Lung Foundation
    1 January 2021 - 31 December 2021
  • Swedish Heart-Lung Foundation
    1 January 2021 - 31 December 2023
  • Swedish Heart-Lung Foundation
    1 January 2021 - 31 December 2021
  • Swedish Heart-Lung Foundation
    1 January 2019 - 31 December 2020
  • Swedish Heart-Lung Foundation
    1 January 2018 - 31 December 2020
  • Swedish Research Council
    1 January 2018 - 31 December 2021

Employments

  • Principal Researcher, Department of Molecular Medicine and Surgery, Karolinska Institutet, 2022-
  • Graduate researcher, Institute for Molecular Genetics and Genetic Engineering, 2002-2003

Degrees and Education

  • Docent, Karolinska Institutet, 2021
  • Degree Of Doctor Of Philosophy, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 2012

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