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  • Journal article
    Marei I, Vinokurova M, Qiucheng L, Nyhegn L, Dubuis E, Baig A, Mohamed N, Rothery S, Kirkby NS, Salem V, Oliver N, Mitchell JA, AhmetajShala Bet al., 2025,

    Impact of type 1 diabetes on endothelial cells derived from living donors

    , FASEB BioAdvances, Vol: 7, ISSN: 2573-9832

    Endothelial colony forming cells (ECFCs) derived from peripheral blood have been shown to retain disease phenotype in several conditions thus possessing great translational potential for regenerative medicine. Hyperglycaemia may alter the phenotype of ECFCs yet the characteristics of ECFCs isolated from people with type 1 diabetes (T1D) have not been described. Here, we establish whether ECFCs can be successfully isolated from donors with T1D and we characterize their functional properties. Human ECFCs were isolated from peripheral blood of up to 9 control and T1D donors. Expression of cell markers and cytokines was analyzed using immunocytochemistry, RT-PCR and ELISA. Ca2+ signaling and contraction were studied using Fluo-4-AM in cells treated with serial concentrations of histamine (1 × 10−7-1 × 10−4M). T1D ECFCs showed robust endothelial marker expression and displayed normal morphology but had a reduced size compared to those from control donors. In response to inflammatory stimuli, T1D ECFCs exhibited exaggerated pro-atherogenic/pro-inflammatory cytokine (IL-6 and MCP-1) and adhesion molecule gene induction (VCAM-1 and ICAM-1) but suppressed induction of interferon signaling markers (IP-10). Histamine stimulated a concentration-dependent increase in Ca2+ influx in ECFCs which was significantly reduced in ECFCs from T1D donors, independent of differences in H1 receptor expression levels. Histamine-induced contraction was significantly enhanced in T1D ECFCs. ECFCs from control and T1D donors exhibit distinct phenotypic differences redolent of the vascular pathologies associated with T1D. This establishes the utility of T1D ECFCs for modeling vascular complications but also highlights the need to understand the potential limitations of autologous ECFCs to treat diabetic complications.
  • Journal article
    Ben-Aicha S, Srivastava P, Kararigas G, Devaux Y, Emanueli C, Sopic Met al., 2025,

    Harnessing multiomics technologies and machine learning for advancing personalized theranostic approaches in atherosclerosis

    , PHARMACOLOGICAL REVIEWS, Vol: 77, ISSN: 0031-6997
  • Journal article
    Ficany A, Del Alamo M, Bernabeu C, Shovlin CL, Rossi Eet al., 2025,

    Epistaxis Prevention, Treatment, and Future Perspectives for Hereditary Hemorrhagic Telangiectasia

    , JOURNAL OF CLINICAL MEDICINE, Vol: 14
  • Journal article
    Tsai T, Keulards D, Corradetti S, De Silva R, Tobe A, Miyashita K, Oshima A, Onuma Y, Serruys Pet al., 2025,

    Comparative Analysis of Angiography-Derived Indexes of Microvascular Resistance (IMR) Versus Absolute Resistance in an Core

    , JACC-JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 86, ISSN: 0735-1097
  • Conference paper
    Buschmann E, Van de Hoef T, De Silva R, Patterson T, Banai S, Luyapan J, West N, Verheye Set al., 2025,

    Sex Specific Outcomes of Treating Patients with Refractory Angina with the Coronary Sinus Reducer: One-year outcomes from the REDUCER-I Registry

    , 37th Annual Symposium on Transcatheter Cardiovascular Therapeutics (TCT), Publisher: ELSEVIER SCIENCE INC, ISSN: 0735-1097
  • Journal article
    Woolf B, De Bie E, McLaughlin V, Gräf S, Toshner M, Wilkins MR, Rhodes CJ, Burgess Set al., 2025,

    A cautionary note on the naive use of general-population biobanks to study pulmonary arterial hypertension, with a focus on Mendelian randomization

    , European Respiratory Journal, Vol: 66, ISSN: 0903-1936
  • Journal article
    Wilkins MR, Villar SS, Wason J, Toshner M, Rothman AMKet al., 2025,

    Drug Development for Pulmonary Arterial Hypertension: Unleashing the Potential of Single-Patient Studies Using Continuous Monitoring

    , PULMONARY CIRCULATION, Vol: 15, ISSN: 2045-8932
  • Journal article
    Singh B, Tzoulaki I, Mayr M, 2025,

    Precision medicine requires precision proteomics: discordance between proteomic and clinical assays in UK Biobank

    , CARDIOVASCULAR RESEARCH, ISSN: 0008-6363
  • Journal article
    de Silva R, Cheng K, Henry TD, Perera D, Taqueti VR, Abreu A, Vervaat F, Gulati M, Shimokawa H, Andreotti F, Kaski J-Cet al., 2025,

    Refractory angina: mechanisms and stratified treatment in obstructive and non-obstructive chronic myocardial ischaemic syndromes

    , European Heart Journal, Vol: 46, Pages: 3738-3757, ISSN: 0195-668X

    The diagnosis of refractory angina has conventionally been limited to patients with angina and ischaemia secondary to obstructive atherosclerotic epicardial coronary disease who experience persistent symptoms despite optimal pharmacological and revascularization therapies. It is now well-established that angina may also be caused by ischaemia resulting from coronary microcirculatory disorders, coronary vasospasm, and bridging in the absence of obstructive epicardial coronary disease or after “successful” revascularization. This increasingly prevalent and symptomatic group of patients, with both angina and demonstrable ischaemia, have been excluded from the conventional definition of refractory angina. In patients with obstructive epicardial coronary disease, disturbed microcirculatory and vasomotor function, amongst other ischaemic mechanisms, may account for continuing symptoms despite revascularization. Under-recognition of these mechanisms results in inadequate treatment and symptom persistence. In this review, a redefinition of refractory angina is proposed to include the full spectrum of patients experiencing persistent angina despite current maximal guideline-directed medical and revascularization therapies. Systematic approaches for comprehensive investigation are suggested to identify underlying mechanisms of ischaemia and stratify treatments accordingly. The complex needs of patients with refractory angina are likely best addressed by an inter-disciplinary Angina Heart Team with the aim of improving patient symptoms, quality of life, and clinical outcomes.
  • Journal article
    Yogeswaran A, Hassoun PM, Saleh K, Funderich M, Balasubramanian A, Konswa Z, Kiely DG, Lawrie A, Thenappan T, Eichstaedt CA, Grunig E, Wilkins MR, Howard L, Olschewski H, Kovacs G, Cajigas HR, Frantz R, Sabbour H, Sweatt AJ, Zamanian RT, Arvanitaki A, Giannakoulas G, Elwing J, Jose A, Beckmann S, Olsson KM, Stadler S, Held M, Halank M, Ewert R, Behr J, Milger-Kneidinger K, Pausch C, Pittrow D, Majeed RW, Wilhelm J, Ghofrani HA, Grimminger F, Tello K, Hoeper MM, Seeger W, PVRI GCet al., 2025,

    Hemodynamics and Phosphodiesterase-5 Inhibitor Treatment Associated with Survival in Pulmonary Hypertension in Interstitial Lung Disease A PVRI GoDeep Meta-Registry Analysis

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 211, Pages: 1855-1866, ISSN: 1073-449X
  • Journal article
    Das H, Ironton H, Coote N, Cabuntug JA, Ranger JE, Alsafi A, Shovlin Cet al., 2025,

    Adolescent exercise capacity predicts higher exercise tolerance later in life when compounded by anaemia in patients with pulmonary arteriovenous malformations

    , Thorax, Vol: 80, Pages: 756-760, ISSN: 0040-6376

    Exercise tolerance predicts survival and mental health. To test benefits during adolescence for patients with pulmonary arteriovenous malformations (PAVMs) that cause hypoxaemia, we examined current and retrospective exercise tolerance aged 12y and 19y, linking to clinical records. In the 85 patients (65 female, mean age 56y), current metabolic equivalents ranged from 1.75 to 14.8(mean 7.85) kcal.kg-1.min-1. Oxygen saturation explained only 2.2% of the variability. There were stronger associations between current exercise tolerance and anaemia indices, particularly the need for blood transfusions. In univariate and multivariate analyses, thestrongest anaemia-independent predictor was exercise tolerance aged 19y. In this cohort, the benefit associated with modestly increased activity by 19y (2.9 METs) was greater than the decrements from severe anaemia (~2.54 METs) or 3 decades of life (2.13 METs). The data support enhanced exercise for people with PAVMs, as for the general population, in preparation for later-life health challenges.
  • Journal article
    Mahomed AS, Burke-Gaffney A, Moledina S, Toe QK, Dongmin S, Quinlan GJ, Rhodes CJ, Pease JE, Wort Set al., 2025,

    SOX17-silenced HPAECs upregulate NF-κB-induced CXCL10 and CXCL11: implications for lymphocyte chemotaxis in SOX17-PAH

    , Scientific Reports, Vol: 15, ISSN: 2045-2322

    Pulmonary arterial hypertension (PAH) is a progressive pulmonary vasculopathy characterized by extensive pre-capillary arterial remodeling, instigating increased pulmonary vascular resistance and eventual right heart failure. Rare mutations in the SOX17 gene and common variants in the enhancer region are thought to predispose to PAH. Central to the PAH pathobiology is lung immune cell recruitment, orchestrated by the overproduction of chemokines (e.g. CXCL10) via the induction of NF-κB. Emerging evidence from murine models of SOX17 impairment suggests perivascular leukocyte accumulation in the lung, likely due to disordered inflammatory mediator expression. Therefore, in the current study we assessed the role of SOX17 deficiency in human pulmonary artery endothelial cells (HPAECs) on selected inflammatory mediator release. Following a semi-quantitative array of 100 cytokines and chemokines, we identified markedly elevated CXCL10 and CXCL11 mRNA and soluble protein release in SOX17-silenced HPAECs (versus control siRNA-treated cells), driven by excessive NF-κB p65 activity. Further, we show that plasma CXCL10 levels are raised in a small cohort (n = 3) of carriers of pathogenic SOX17 rare variants versus healthy controls. Finally, SOX17 knockdown HPAEC supernatants mediated the in vitro migration of transfectants expressing CXCR3. Therefore, enhanced lymphocyte migration may be a pathomechanism of PAH due to SOX17 loss, driven by a CXCL10/CXCL11/CXCR3 axis.
  • Journal article
    Carulli E, McGarvey M, Chabok M, Panoulas V, Rosser G, Akhtar M, Smith R, Chandra N, Al-Hussaini A, Kabir T, Barker L, Bruno F, Konstantinou K, de Silva R, Hill J, Xu Y, Lane R, Bucciarelli-Ducci C, Luescher T, Dalby Met al., 2025,

    Transcoronary cooling and dilution for cardioprotection during revascularisation for ST-segment elevation myocardial infarction: design and rationale of the STEMI-Cool study (vol 282, pg 40, 2025)

    , AMERICAN HEART JOURNAL, Vol: 288, ISSN: 0002-8703
  • Journal article
    Yarmolinsky J, Lau E, Koskeridis F, Gunter MJ, Wang D, Dehghan A, Tzoulaki Iet al., 2025,

    Genome-Wide Pleiotropy Analysis Identifies Shared and Opposing Pathways Influencing Coronary Artery Disease and Cancer

    , ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 45, Pages: 1945-1956, ISSN: 1079-5642
  • Journal article
    Zoodsma M, Beuchel C, Yasmeen S, Kohleick L, Nepal A, Koprulu M, Kronenberg F, Mayr M, Williamson A, Pietzner M, Langenberg Cet al., 2025,

    A genetic map of human metabolism across the allele frequency spectrum

    , NATURE GENETICS, Vol: 57, ISSN: 1061-4036
  • Journal article
    Ma E, Schafer CM, Xie J, Rudenko Y, Knapp JTH, Randi AM, Birdsey GM, Griffin CTet al., 2025,

    Targeting endothelial ERG to mitigate vascular regression in retinopathies

    , Proceedings of the National Academy of Sciences, Vol: 122, ISSN: 0027-8424

    Retinopathy of prematurity (ROP) and diabetic retinopathy (DR) are ocular disorders in which an initial loss of retinal capillaries leads to damaging tissue ischemia followed by a compensatory neovascularization response that generates pathological capillaries in the eye. Using a mouse model of ROP and samples from DR patients, we found that the highly homologous and homeostatic erythroblast transformation-specific (ETS) family transcription factors ETS-related gene (ERG) and Friend leukemia integration 1 (FLI1) are downregulated in endothelial cells (ECs) of retinal capillaries prior to their regression in early stages of these diseases. We developed a mouse model of inducible EC-specific overexpression of Erg and found it mitigates capillary regression, retinal neuron death, neovascularization, and visual defects in the ROP model. Erg overexpression also reduces capillary regression in early stages of a murine DR model. We next found that simultaneous deletion of endothelial Erg and Fli1 is sufficient to promote regression of the pathological retinal capillaries that arise in late stages of the ROP model. Altogether, our data demonstrate that deletion of homeostatic endothelial ETS factors promotes capillary regression, while maintenance of even one of these factors prevents regression. These findings offer insights into approaches for preventing and treating retinopathies at different stages of these diseases.
  • Journal article
    O'Brien D, Alhathli E, Harwood C, Bhattacharya D, Gupta K, Julian T, Weinreich M, West RJH, Wang D, Byrne RP, McLaughlin RL, Wuu J, Benatar M, Cooper-Knock J, Shaw PJet al., 2025,

    Extreme exercise in males is linked to mTOR signalling and onset of amyotrophic lateral sclerosis

    , BRAIN, ISSN: 0006-8950
  • Journal article
    Mueller C, White HD, Lopez-Ayala P, de Silva R, Kaski JCet al., 2025,

    Great debate: the universal definition of myocardial infarction is flawed and should be put to rest

    , EUROPEAN HEART JOURNAL, ISSN: 0195-668X
  • Journal article
    Nicoleau S, Valle YR, Tura-Ceide O, Armour CH, Barbera JA, McKinnon TAJ, Gopalan D, Wojciak-Stothard Bet al., 2025,

    3D modelling of pulmonary arterial stenosis and endothelial dysfunction in CTEPH

    , Lab on a Chip: miniaturisation for chemistry, physics, biology, materials science and bioengineering, Vol: 25, Pages: 4369-4384, ISSN: 1473-0189

    Chronic thromboembolic pulmonary hypertension (CTEPH) arises from progressive thrombotic occlusion of pulmonary arteries, involving vessel blockage by unresolved thrombi and small vessel arteriopathy. This disrupts blood flow, increases lung pressure, and alters vessel geometry, contributing to endothelial dysfunction. However, the mechanisms remain unclear. To study these interactions, we developed microfluidic 3D models of pulmonary arteries with 30–80% stenosis using CTPAs from CTEPH and acute pulmonary embolism (APE) patients, in silico flow simulations, 3D printing, and soft lithography. Unlike standard circular channels, we designed semi-circular channels enclosed by a coverslip, which computational modelling confirmed closely mimics real vessel flow dynamics. Human pulmonary artery endothelial cells (HPAECs) cultured in 30–80% stenosis channels exhibited increased expression of pro-inflammatory, pro-thrombotic, and pro-angiogenic genes, with responses varying by stenosis severity and location. Cells in post-stenotic dilatation regions (60–80% stenosis) lost alignment and junctional integrity due to disturbed flow. The transcriptional profile of HPAECs from 80% stenosis channels closely resembled that of CTEPH pulmonary endarterectomy specimens. Platelet adhesion, dependent on von Willebrand factor (VWF), varied with stenosis severity and flow rate. Low perfusion rates increased adhesion in stenotic regions, while higher flow rates promoted adhesion post-stenosis. Our patient data-based stenosis models provide a robust platform for studying the effects of vascular geometry on blood flow, endothelial responses, and platelet aggregation, advancing research on CTEPH, pulmonary embolism, and other diseases associated with vascular occlusion.
  • Journal article
    Prasad M, Konigstein M, de Silva R, Lerman A, Banai S, De Silva Pet al., 2025,

    Principles of Coronary Sinus Narrowing to Relieve Myocardial Ischemia and Improve Angina

    , American Journal of Cardiology, ISSN: 0002-9149

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