Dr Jovana Serbanovic-Canic
School of Medicine and Population Health
Lecturer in Cardiovascular Science
+44 114 215 9502
Full contact details
School of Medicine and Population Health
The Medical School
Beech Hill Road
Sheffield
S10 2RX
- Profile
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I am a Lecturer in Cardiovascular Science at the University of Sheffield, where I lead a research programme investigating how mechanical forces generated by blood flow shape vascular health and contribute to cardiovascular disease.
Cardiovascular disease remains the leading cause of death worldwide, yet many fundamental questions remain about why vascular disease develops at specific sites within the circulation and how disease progresses. My research seeks to understand how blood vessels sense and respond to mechanical cues such as blood flow, pressure and stretch, and how disruption of these processes drives vascular dysfunction.
My group focuses on vascular mechanobiology, with a particular interest in endothelial cells, the specialised cells that line the inside of blood vessels and act as key regulators of vascular homeostasis. We investigate how endothelial cells communicate with neighbouring vascular smooth muscle cells and other components of the vessel wall to regulate inflammation, barrier function, cell survival and vascular remodelling.
By combining mechanistic vascular biology with translational models of disease, our work aims to identify novel pathways that contribute to atherosclerosis, aneurysm development and other cardiovascular disorders, with the long-term goal of informing future therapeutic strategies.
Prior to my appointment as Lecturer, I held a British Heart Foundation Intermediate Basic Science Research Fellowship at the University of Sheffield, where I established an independent research programme investigating endothelial responses to disturbed blood flow in atherosclerosis. I completed my PhD as a Marie Curie Fellow at the University of Cambridge, studying the functional genomics of blood cell development.
- Research interests
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My group investigates how mechanical forces regulate vascular cell behaviour in health and disease. Blood vessels are constantly exposed to forces generated by blood flow, pressure and stretch. Endothelial cells sense these mechanical cues and convert them into biological signals that control inflammation, permeability, cell survival and communication with neighbouring cells. Disruption of these processes contributes to cardiovascular diseases such as atherosclerosis and aortic aneurysms.
Current research interests include:
Endothelial mechanosensing in cardiovascular disease
We investigate how endothelial cells sense mechanical forces generated by blood flow, particularly in regions of disturbed flow where vascular disease commonly develops. We are interested in the molecular pathways that link mechanical force to endothelial dysfunction, inflammatory activation, apoptosis, permeability and vascular remodelling.
PKD1-dependent vascular signalling
A major focus of the group is polycystin-1, encoded by PKD1. PKD1 is best known for its role in autosomal dominant polycystic kidney disease, but cardiovascular complications are common in this condition and the underlying mechanisms remain poorly understood. Our work investigates how PKD1 regulates endothelial responses to mechanical force and how PKD1-dependent pathways contribute to vascular dysfunction, atherosclerosis and aneurysm biology.
Extracellular matrix remodelling and vascular wall dysfunction
Changes in extracellular matrix composition and organisation are central to vascular remodelling, plaque development and aneurysm formation. We investigate how endothelial mechanosensing pathways regulate extracellular matrix-associated molecules and how these changes contribute to structural weakening or dysfunction of the vessel wall.
Translational vascular models and data-driven biology
Our research combines mechanistic vascular biology with disease-relevant experimental systems and molecular analysis. Approaches used in the group include in vivo and in vitro models, flow-based assays, gene silencing, fluorescence microscopy, immunostaining, qPCR, protein-based assays, image analysis, bioinformatics and cutting edge -omics approaches. Through collaborations with clinical and basic science researchers, we aim to translate fundamental discoveries into clinically relevant insights for cardiovascular disease.
- Publications
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Show: Featured publications All publications
Featured publications
Journal articles
- Sensing of shear stress in vascular endothelial cells – from physiology to pathology. Journal of Cell Science, 139(7). View this article in WRRO
- TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques. Nature Communications, 17. View this article in WRRO
- Endothelial c-REL orchestrates atherosclerosis at regions of disturbed flow through crosstalk with TXNIP-p38 and non-canonical NF-κB pathways. Cardiovascular Research, 121(5), 748-759. View this article in WRRO
- EVA1A (eva-1 homolog A) promotes endothelial apoptosis and inflammatory activation under disturbed flow via regulation of autophagy. Arteriosclerosis, Thrombosis, and Vascular Biology, 43(4), 547-561. View this article in WRRO
- JAG1-NOTCH4 mechanosensing drives atherosclerosis. Science Advances, 8(35). View this article in WRRO
- Shear stress induces endothelial-to-mesenchumal transition via the transcription factor Snail. Scientific Reports, 7. View this article in WRRO
- Zebrafish Model for Functional Screening of Flow-Responsive Genes.. Arteriosclerosis, Thrombosis, and Vascular Biology. View this article in WRRO
- New gene functions in megakaryopoiesis and platelet formation. Nature, 480(7376), 201-208.
- Silencing of RhoA nucleotide exchange factor, ARHGEF3, reveals its unexpected role in iron uptake.. Blood, 118(18), 4967-4976.
All publications
Journal articles
- Sensing of shear stress in vascular endothelial cells – from physiology to pathology. Journal of Cell Science, 139(7). View this article in WRRO
- TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques. Nature Communications, 17. View this article in WRRO
- Endothelial c-REL orchestrates atherosclerosis at regions of disturbed flow through crosstalk with TXNIP-p38 and non-canonical NF-κB pathways. Cardiovascular Research, 121(5), 748-759. View this article in WRRO
- Zebrafish model for functional screening of flow-responsive genes controlling endothelial cell proliferation. Scientific Reports, 14(1). View this article in WRRO
- EPAS1 Attenuates Atherosclerosis Initiation at Disturbed Flow Sites Through Endothelial Fatty Acid Uptake. Circulation Research, 135(8), 822-837.
- Controversy in mechanotransduction: the role of endothelial cell-cell junctions in fluid shear stress sensing. Journal of Cell Science, 137(17). View this article in WRRO
- DLL4 promotes partial endothelial-to-mesenchymal transition at atherosclerosis-prone regions of arteries. Vascular Pharmacology, 150, 107178-107178.
- EVA1A (eva-1 homolog A) promotes endothelial apoptosis and inflammatory activation under disturbed flow via regulation of autophagy. Arteriosclerosis, Thrombosis, and Vascular Biology, 43(4), 547-561. View this article in WRRO
- JAG1-NOTCH4 mechanosensing drives atherosclerosis. Science Advances, 8(35). View this article in WRRO
- Zebrafish as a tractable model of human cardiovascular disease. British Journal of Pharmacology, 179(5), 900-917. View this article in WRRO
- Quantifying endothelial cell proliferation in the zebrafish embryo. F1000Research, 10. View this article in WRRO
- The effect of absent blood flow on the zebrafish cerebral and trunk vasculature. Vascular Biology, 3(1), 1-16. View this article in WRRO
- Shear stress : the dark energy of atherosclerotic plaques. Cardiovascular Research, 117(8), 1811-1813. View this article in WRRO
- Shear stress induces endothelial-to-mesenchymal transition via the transcription factor Snail (vol 7, 3375, 2017). SCIENTIFIC REPORTS, 10(1).
- Endothelial responses to shear stress in atherosclerosis: a novel role for developmental genes. Nature Reviews Cardiology, 17(1), 52-63.
- Homeobox B9 integrates bone morphogenic protein 4 with inflammation at atheroprone sites. Cardiovascular Research. View this article in WRRO
- Shear stress makes its mark on the endothelial genome. Cardiovascular Research, 115(10), 1449-1451. View this article in WRRO
- β1 integrin is a sensor of blood flow direction. Journal of Cell Science, 132(11). View this article in WRRO
- GATA4-Twist1 signalling in disturbed flow-induced atherosclerosis. Cardiovascular Drugs and Therapy, 33(2), 231-237. View this article in WRRO
- β1 integrin is a sensor of blood flow direction.
- Shear stress induces endothelial-to-mesenchumal transition via the transcription factor Snail. Scientific Reports, 7. View this article in WRRO
- Zebrafish Model for Functional Screening of Flow-Responsive Genes.. Arteriosclerosis, Thrombosis, and Vascular Biology. View this article in WRRO
- Experimental Approaches to Study Endothelial Responses to Shear Stress. Antioxidants & Redox Signaling, 25(7), 389-400.
- TWIST1 Integrates Endothelial Responses to Flow in Vascular Dysfunction and Atherosclerosis.. Circulation Research, 119, 450-462. View this article in WRRO
- A loss of function screen of identified genome-wide association study Loci reveals new genes controlling hematopoiesis.. PLoS Genet, 10(7), e1004450.
- Mechanoresponsive networks controlling vascular inflammation.. Arterioscler Thromb Vasc Biol, 34(10), 2199-2205.
- Loss of function of parathyroid hormone receptor 1 induces Notch-dependent aortic defects during zebrafish vascular development.. Arterioscler Thromb Vasc Biol, 33(6), 1257-1263.
- Image-based characterization of thrombus formation in time-lapse DIC microscopy.. Med Image Anal, 16(4), 915-931.
- New gene functions in megakaryopoiesis and platelet formation. Nature.
- New gene functions in megakaryopoiesis and platelet formation. Nature, 480(7376), 201-208.
- Joint thrombus and vessel segmentation using dynamic texture likelihoods and shape prior.. Med Image Comput Comput Assist Interv, 14(Pt 3), 579-586.
- Silencing of RhoA nucleotide exchange factor, ARHGEF3, reveals its unexpected role in iron uptake.. Blood, 118(18), 4967-4976.
- The role of meis1 in primitive and definitive hematopoiesis during zebrafish development.. Haematologica, 96(2), 190-198.
- A genome-wide meta-analysis identifies 22 loci associated with eight hematological parameters in the HaemGen consortium.. Nat Genet, 41(11), 1182-1190.
Conference proceedings
- The role of polycystin-1 in endothelial dysfunction and cardiovascular disease. JOURNAL OF VASCULAR RESEARCH, Vol. 62(SUPPL 1)
- BS1 Polycystin-1 suppresses apoptotic signalling in endothelial cells and protects from atherosclerosis. Basic Science (pp A247.1-A247)
- BS15 Using zebrafish embryos to identify genes that regulate endothelial proliferation. Basic science (pp A163.2-A164)
- Mechanosensitive Hox Genes Control Vascular Dysfunction in Adult Arteries. CARDIOVASCULAR DRUGS AND THERAPY, Vol. 33(2) (pp 272-272)
- The Role of FAM176A in Endothelial Cell Responses to Flow. CARDIOVASCULAR DRUGS AND THERAPY, Vol. 33(2) (pp 273-273)
- YIA4: IDENTIFICATION OF NOVEL SHEAR STRESS-RESPONSIVE REGULATORS OF ENDOTHELIAL CELL DYSFUNCTION USING THE ZEBRAFISH MODEL. Heart, Vol. 99(suppl 2) (pp A6.1-A6)
- Silencing of RhoA nucleotide exchange factor, ARHGEF3, reveals its role in thrombopoiesis and iron uptake. JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol. 9 (pp 33-33)
- Thrombus segmentation by texture dynamics from microscopic image sequences. Progress in Biomedical Optics and Imaging Proceedings of SPIE, Vol. 7623(PART 1)
- THE ROLE OF MEIS1 IN PRIMITIVE AND DEFINITIVE HAEMATOPOIESIS AND VASCULAR PATTERNING DURING ZEBRAFISH DEVELOPMENT. HAEMATOLOGICA-THE HEMATOLOGY JOURNAL, Vol. 95 (pp 247-247)
Preprints
- TWIST1 drives endothelial-to-mesenchymal-transition to stabilize atherosclerotic plaques, Cold Spring Harbor Laboratory.
- EPAS1 Attenuates Atherosclerosis Initiation at Disturbed Flow Sites through Endothelial Fatty Acid Uptake, Cold Spring Harbor Laboratory.
- The effect of absent blood flow on the zebrafish cerebral and trunk vasculature, Cold Spring Harbor Laboratory.
- JAG1-NOTCH4 Mechanosensing Drives Atherosclerosis, Cold Spring Harbor Laboratory.
- Sensing of shear stress in vascular endothelial cells – from physiology to pathology. Journal of Cell Science, 139(7). View this article in WRRO
- Research group
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- Mr George Bowley (NC3R PhD Studentship)
- Mr Samuel Sendac (Research Technician)
I am always keen to hear from enthusiastic and motivated scientists interested in cardiovascular biology, vascular mechanobiology and translational vascular research.
Our laboratory offers a collaborative and supportive research environment where students and researchers can develop expertise in experimental vascular biology, advanced imaging, bioinformatics and cutting-edge multi-omics approaches.
Researchers in the group gain experience in:
- Experimental models of cardiovascular disease
- Endothelial and vascular cell biology
- Flow-based mechanobiology systems
- Advanced fluorescence microscopy
- Molecular and cellular biology techniques
- Bioinformatics and transcriptomic analysis
- Scientific writing, presentation and grant development
Our aim is to provide interdisciplinary training that prepares researchers for careers in academia, biotechnology, pharmaceutical science and related sectors.
Self-Funded PhD Students & Scholarship Applicants
I strongly encourage enquiries from prospective PhD students who are self-funded or planning to apply for national, governmental or international scholarship schemes.
If you are passionate about cardiovascular science and interested in pursuing doctoral research in one of the areas above, I would be delighted to discuss potential research projects and support your application.
Prospective applicants should email:
- A current CV
- A brief description of their research interests
- Details of any existing or planned funding arrangements
- Teaching activities
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MBChB Phase 1 Cardiovascular Block Lead
- Professional activities and memberships
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Honorary Treasurer of the British Society for Cardiovascular Research (BSCR)
Member of the British Atherosclerosis Society (BAS)