About

Professor Katya Ravid, DSc, FAAAS and FAHA, holds the Barbara E. Corkey Professorship of Medicine and is a Professor of Biochemistry, Biology, and Health Sciences at Boston University Chobanian & Avedisian School of Medicine. She is the Founding Director of both the BU Interdisciplinary Biomedical Research Office (BU IBRO) and the Evans Center for Interdisciplinary Biomedical Research (ECIBR), as well as an Investigator at the Whitaker Cardiovascular Institute (WCVI). Dr. Ravid received her training at the Technion and MIT and is recognized as an Established Investigator and Fellow of the American Heart Association. She has contributed extensively to the scientific community by serving on editorial and advisory boards, participating in ASH and Purines Scientific Committees, and chairing prominent conferences such as the Gordon Research Conference on the cell biology of megakaryocytes and platelets. Her research and teaching excellence have been acknowledged through numerous awards, including the Boston University Chobanian & Avedisian School of Medicine Educator of the Year Award in Graduate Medical Sciences, the Sidney University Professorship Award, the Weizmann Institute Rosi and Max Varon Professorship Award, and the Fulbright Scholar Award as a long-standing ASMBM member. Additionally, she directs the NHLBI-funded Training Program in Cardiovascular Biology, underscoring her commitment to advancing cardiovascular research and education. Professor Ravid's work is characterized by a dedication to creativity, tenacity, and generosity, which she identifies as the foundation of rewarding science.

Research topics

• Internal medicine
• Biology
• Medicine
• Endocrinology
• Cell biology
• Chemistry
• Cancer research
• Bioinformatics
• Immunology

Selected publications

• Tryptophan metabolism reprogramming potentially contributes to the prothrombotic milieu in mice and humans with SARS-CoV-2

  Blood Vessels Thrombosis & Hemostasis · 2026-01-05

  articleOpen access

  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection disturbs the coagulation balance in the blood, triggering thrombosis and contributing to organ failure. The role of prothrombotic metabolites in COVID-19-associated coagulopathy remains elusive. Leveraging K18-hACE2 mice infected with SARS-CoV-2, we observed higher levels of the tryptophan metabolite, kynurenine, than in controls. SARS-CoV-2-infected mice showed a significant upregulation of enzymes controlling kynurenine biogenesis, such as indoleamine 2,3-dioxygenase 1 (IDO-1) and tryptophan 2,3-dioxygenase in the kidney and liver, respectively, as well as changes in the enzymes involved in kynurenine catabolism, including kynurenine monooxygenase and kynurinase. Consistent with the agonistic role of these metabolites in aryl hydrocarbon receptor (AHR) signaling, AHR activation and its downstream mediator, tissue factor (TF), a highly potent procoagulant factor, was observed in endothelial cells (ECs) of lungs and kidneys of infected mice. These findings were validated in humans. Compared with controls, sera of patients with COVID-19 showed increased levels of kynurenine, kynurenic acid, anthranilic acid, and quinolinic acid. Activation of the AHR-TF axis was noted in the kidneys and lungs of patients with COVID-19, and sera from patients infected with SARS-CoV-2 showed higher IDO-1 activity than controls. Kynurenine levels in patients with COVID-19 correlated strongly with the TF-inducing activity of sera from patients infected with SARS-CoV-2 on ECs. A specific IDO-1 inhibitor or AHR inhibitor separately or in combination suppressed sera from induced TF activity in ECs from patients with COVID-19. Together, we identified IDO-1 as upregulated by SARS-CoV-2 infection, resulting in augmented kynurenine and its prothrombotic catabolites, thereby suggesting the kynurenine-AHR-TF axis as a potential new diagnostic and therapeutic target.

  PublisherDOI

• A deep learning model to dynamically predict cancer-associated thromboembolism in large-scale healthcare systems

  npj Digital Medicine · 2026-05-18

  articleOpen access

  Venous thromboembolism (VTE) is a leading cause of preventable death among patients undergoing systemic treatment for cancer. Studies suggest that treatment strategies such as direct oral anticoagulant administration can significantly reduce the likelihood of VTE. Therefore, identifying people at high risk is of critical importance. Leveraging electronic health records (EHRs) from the U.S. Veterans Affairs (VA) healthcare system, we developed a transformer model to predict VTE risk in 80,808 cancer patients following the initiation of systemic treatment. The model uses longitudinal diagnostic codes, laboratory values, and demographic data. The proposed transformer model dynamically predicts VTE risk in 3-month quarterly intervals over the year following systemic treatment, achieving progressively improved performance across quarters (AUC: 0.68-0.77). The model is similarly performant on the external validation cohort from the Harris Health System (HHS) with 9752 patients (AUC: 0.68-0.74). By improving its predictions as a patient's history evolves, this dynamic model surpasses prior static risk scores and better supports actionable decisions deeper into the treatment course.

  PublisherOA PDFDOI

• Abstract 4462 IDO1 downregulation by its novel E3 ligase SHFM3 is modulated by Indoxyl Sulfate, exacerbating its prothrombotic effect

  Journal of Biological Chemistry · 2026-05-01

  articleOpen access
  PublisherDOI

• Hematopoietic JAK2V617F mutation-induced reprogramming of blood and bone marrow megakaryocytes

  Blood Advances · 2026-02-18

  articleOpen accessSenior author

  1. Wild type and JAK2 mutated megakaryocytes derived from blood

  PublisherOA PDFDOI

• Piezo1 Mechanosensor Expression in Rare Hematopoietic Cells Controls Systemic Inflammatory Response in Mice

  Cells · 2025-12-16

  articleOpen accessSenior author

  Mutations in the Piezo1 mechanosensor are associated with blood cell anomalies. The objective of our study was to explore the role of Piezo1 in the development and function of the megakaryocyte (MK) lineage. To this end, PF4-Cre mice, bearing Cre recombinase under the control of the Pf4 gene promoter—which drives expression to hematopoietic progenitors and to the MK/platelet lineage—were crossbred with Piezo1-floxed mice to generate Piezo1 knockout (KO) mice. In our results, the hematopoietic stem cell (HSC) count—including Multipotent Progenitors 2 (MPP2) progenitors that give rise to MKs—tended to be augmented in KO mice, while the level of MPP3 progenitors that give rise to white blood cells (WBCs) tended to be reduced, as compared to matching controls. The level of circulating WBCs was significantly reduced in the KO mice compared to controls. In addition, while platelet count was modestly elevated, platelet activation response was reduced in Piezo1 KO mice compared to controls. MK levels and ploidy were similar in both groups. Baseline serum pro-and anti-inflammatory cytokine profiles were also similar in the two experimental groups. However, upon LPS challenge, there was a significant reduction in IL-6 and INF-γ levels in the sera of Piezo1 KO mice compared to controls. Our findings point to an immunoregulatory and thrombotic potential of Piezo1 in relatively rare bone marrow cells, along with an ability to modulate WBC count.

  PublisherOA PDFDOI

• A panel of plasma proteins associated with venous thromboembolism in patients with prostate cancer

  Cancer Biomarkers · 2025-12-01

  articleOpen accessCorresponding

  PurposeVenous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism, is a leading cause of morbidity and mortality in cancer patients. Prostate cancer is associated with an elevated risk of VTE, yet the molecular drivers remain poorly defined.MethodsIn this study, we employed high-throughput proteomic profiling using the SomaLogic platform to analyze plasma from 85 prostate cancer patients, including 43 with and 42 without VTE. Samples were collected at cancer diagnosis, with VTE diagnosed at a mean of 96.8 months later.ResultsPrincipal component analysis showed modest proteomic separation between groups. Differential expression analysis identified enriched pathways in VTE patients, including hemostasis (TIMP1, JAM2, TMX3, F3, and ESAM), cell adhesion (CXCL12, CCL11, CCN5, COL18A1, and ADGRB1) and cell proliferation (TIMP1, REG1B, REG1A, CRLF2, and ALDH1A2). Receiver Operating Characteristic analysis using top fifteen proteins achieved an area under the curve of 0.859, indicating strong predictive value for VTE in this cohort.ConclusionsWe identified a specific cluster of circulating proteins associated with development of VTE in patients with prostate cancer. This work deepens understanding of systemic mediators of cancer-associated VTE and, pending validation in other cohorts, paves the way for improved risk stratification and long-term monitoring in this population.

  PublisherDOI

• Immune and Inflammatory Properties of Megakaryocytes

  Cells · 2025-07-10 · 3 citations

  reviewOpen accessSenior author

  Megakaryocytes (MKs), which primarily develop in bone marrow (BM) from hematopoietic stem cells, are critical for platelet production. Beyond their well-established role in thrombopoiesis, MKs have been identified as important for BM niche maintenance, such as by supporting the growth and differentiation of other cell types. Recently, megakaryopoiesis has been reported as yielding divergent subpopulations of MKs, as evidenced by single-cell RNA sequencing of lung, spleen, or BM resident MKs. Interestingly, these subpopulations constitute a significant proportion of "immune MKs" expressing various classical immune markers and capable of phagocytosing pathogens and contributing to antigen presentation. As such, MKs were also found to regulate inflammation, mainly by secreting various cytokines and chemokines to crosstalk with other cell types. The level and functional signature of these "immune MKs" were found to be altered in various pathological conditions, indicative of their purposeful values in health and diseases. In this review, we survey and highlight newly reported functional immune and inflammatory properties of MKs in health and in select pathologies.

  PublisherDOI

• Tryptophan metabolism reprogramming contributes to the prothrombotic milieu in mice and humans infected with SARS-CoV-2

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-21 · 1 citations

  preprintOpen access

  SARS-CoV-2 infection disturbs the coagulation balance in the blood, triggering thrombosis and contributing to organ failure. The role of prothrombotic metabolites in COVID-19-associated coagulopathy remains elusive. Leveraging K18-hACE2 mice infected with SARS-CoV-2, we observed higher levels of the tryptophan metabolite, kynurenine, compared to controls. SARS CoV-2 infected mice showed a significant upregulation of enzymes controlling Kynurenine biogenesis, such as indoleamine 2,3-dioxygenase (IDO-1) and tryptophan 2,3-dioxygenase levels in kidneys and liver, respectively, as well as changes in the enzymes involved in kynurenine catabolism, including kynurenine monooxygenase and kynurinase. Consistent with the agonistic role of these metabolites in Aryl Hydrocarbon Receptor (AHR) signaling, AHR activation and its downstream mediator, tissue factor (TF), a highly potent procoagulant factor, was observed in endothelial cells (ECs) of lungs and kidneys of infected mice. These findings were validated in humans, where compared to controls, sera of COVID-19 patients showed increased levels of Kynurenine, kynurenic acid, anthranilic acid, and quinolinic acid. Activation of the AHR-TF axis was noted in the kidneys and lungs of COVID-19 patients, and COVID-19 sera showed higher IDO-1 activity than controls. Levels of Kyn in COVID-19 patients correlated strongly with the TF inducing activity of COVID-19 sera on ECs. A specific IDO-1 inhibitor or AHR inhibitor separately or in combination suppressed COVID-19 sera-induced TF activity in ECs. Together, we identified IDO-1 as upregulated by SARS-CoV-2 infection, resulting in augmented Kyn and its prothrombotic catabolites, thereby suggesting the Kyn AHR-TF axis as possibly a new diagnostic and/or therapeutic target.

  PublisherOA PDFDOI

• A deep learning model to dynamically predict cancer-associated thrombosis using electronic health records from the u.s. veterans affairs healthcare system

  Blood · 2025-11-03

  articleOpen access

  Abstract Background: Venous thromboembolism (VTE) is a potentially preventable complication in cancer patients undergoing systemic therapy. Randomized controlled trials have shown that administration of prophylactic anticoagulants may mitigate this risk. As such, real-time and dynamic identification of patients at risk of VTE at any given point in time is critical. Artificial intelligence/machine learning (AI/ML) methods that can integrate a large amount of complex information that accrues over the patient's history are well-suited to this task. Methods: Data for this study were derived from the Corporate Data Warehouse (CDW) of the Veterans Affairs (VA) healthcare system in the US. We used all cancer patients within the VA Cancer Registry from 2006 to 2022 and assigned 80,808 patients with systemic treatment initiation dates from 2011-20 to the primary cohort, and 3,303 from 2021-22 as the temporal validation cohort. Patients were further excluded if they were not primary users of the VA healthcare system, received prior anticoagulation, or had recent VTE diagnoses within 6 months of systemic treatment. We developed a novel transformer-based AI/ML model with event-feature embedding and multi-headed attention layers that predicts future VTE within one year of systemic treatment. Longitudinal patient trajectories comprised of time-stamped diagnostic codes (phecodes) and laboratory records from the patient's medical history were constructed to predict VTE risk. Input trajectories comprised of 1,862 distinct phecodes, which are synoptic concepts derived from diagnostic ICD codes and 18 laboratory tests derived from the complete blood cell count and metabolic panels. Sex, race, and BMI were included as static covariates. Cancer diagnosis dates and treatment index dates were used as anchor times to account for the relative positional encoding of events with respect to these points in the patient's history. The transformer-based AI/ML model used four distinct input trajectories of phecodes and labs to predict VTE risk in four consecutive quarterly look-forward windows following the initiation of systemic treatment. For each patient, input trajectories started at 3 months before the index date and ended at 0, 3, 6, and 9 months after treatment initiation. Corresponding look-forward prediction windows were constructed at (Q1) 0-3, (Q2) 3-6, (Q3) 6-9, and (Q4) 9-12 months beyond the treatment index date. If a patient experienced VTE at a given quarter, they were considered a positive case for that quarter and excluded from subsequent prediction intervals. Patients in the primary cohort were split into training, development, and test sets in a ratio of 60:20:20. The transformer was developed using the training and development sets with a logistic loss function and balanced sampling. Model performance was assessed using area under the receiver operating characteristic curve (AUC). Results: Of the 80,808 patients from the primary cohort, 4,873 (6%) cases of VTE occurred within one year of treatment index date. The incidence of VTE decreased over time, with 3.2% of cases occurring in the first quarter (Q1) after treatment index date, 1.7% in Q2, 1.1% in Q3, and 0.9% in Q4. Test set predictions yielded AUCs of .68, .68, .71, and .77 respectively for Q1-Q4 with recall (sensitivity) rates of .82, .81, .78, and .84 after spline recalibration. Performance was largely consistent across subgroups defined by cancer type, treatment type, and demographics. AUCs were .65, .60, .76, .76 from Q1-Q4 in the temporal validation cohort. Compared to existing clinical risk prediction tools, specifically the widely used Khorana score (Khorana et al., 2005) and EHR-CAT (Li et al., 2023), the transformer model performed similarly in Q1-Q2 but significantly increased identification of high-risk patients up to 50% at Q3-Q4 (6-12 months) past treatment initiation. Conclusion: By leveraging disease histories and lab records data from the comprehensive EHR from the VA CDW, our proposed transformer-based AI/ML model is an effective method to predict VTE risk using disease and lab trajectories. This novel AI/ML model is uniquely suited for dynamic risk assessment with the ability to incorporate pertinent time-dependent information along the entire treatment trajectory.

  PublisherOA PDFDOI

• Lysyl oxidases directly control cell surface abundance of platelet-derived growth factor receptors and signaling in osteoblasts

  Blood · 2025-11-03

  articleOpen accessSenior author

  Abstract Introduction Platelet-derived Growth Factor Receptors α and β (PDGFRs) are fundamental regulators of cell development and differentiation in the bone marrow, supporting hematopoiesis, angiogenesis and bone formation. The osteoblast niche is a significant regulator of myeloid differentiation, and signaling through osteoblast PDGFRs contributes to bone marrow fibrosis by driving stromal proliferation as well as the deposition and cross-linking of extracellular matrix proteins. Consequently, PDGFRs are strongly involved in the progression of myeloproliferative neoplasms (MPN). Lysyl oxidases (LOX, LOXL1-4) are a family of enzymes that facilitate collagen and elastin cross-linking through oxidation of the lysine side chains in these matrix proteins. We previously reported that LOX is upregulated in MPN and can oxidize PDGFRs to enhance signaling and cellular proliferation. While this provides an interesting route for pharmacological intervention in the treatment of hematological malignancies, the various contributory cellular mechanisms/pathways have not been fully explored. Objective The aim of this study was to interrogate the effects of amsulostat (previously called SNT-5505 or PXS-5505), a small molecule lysyl oxidase inhibitor currently in a Phase 2 clinical trial for the treatment of MPN (NCT04676529) on oxidation of lysyl residues within mitogenic growth factor receptors and the regulation of PDGF downstream signalling events. Methods The extracellular moieties of several recombinant growth factor receptors [including PDGF, Vascular Endothelial Growth Factor Receptor (VEGFR) and Epidermal Growth Factor Receptor (EGFR)] were incubated with recombinant lysyl oxidase like 2 (LOXL2) in the presence and absence of amsulostat. Receptor oxidation was measured by fluorescent aldehyde scavenger probes or mass spectrometry. To explore the impact of lysyl oxidases on osteoblast signaling, the human osteosarcoma cell line MG-63, which displays osteoblast-like characteristics, was chosen as it expresses PDGFR α and β. As MG-63 cells secrete low amounts of lysyl oxidases, they were cultured in the presence of amsulostat for 5 days. The media was then replaced with the addition of recombinant LOXL2 in the presence or absence of amsulostat for 24 hours. PDGFR was then stimulated with its ligand PDGFab and cell surface expression was determined using biotinylated membrane-impermeable reagents (sulfo-NHS-SS-biotin). The extracts as well as downstream signaling were measured by a modified version of Western blotting (Jess, BioTechne). All measurements were normalized against unphosphorylated or total proteins as appropriate. Results Amsulostat prevented the formation of aldehydes at the extracellular moiety of three growth factors, including PDGFR, VEGFR and EGFR, suggestive of a common structural feature. Despite the heterogeneous structure of the growth factor receptors, the oxidation of lysine residues occurs in areas related to ligand binding and receptor arrangement. As anticipated from previous reports, PDGFab stimulation of MG-63 cells caused a reduction in the cellular surface expression of PDGFRs. Here, we found that this was more pronounced when lysyl oxidase activity was blocked by amsulostat, importantly suggesting that active LOX preserves this receptor access to its ligand. Accordingly, intracellular signalling was analysed after PDGFR stimulation with PDGFab. The presence of LOX activity enhanced MEK phosphorylation when compared to conditions in which the activity was blocked by amsulostat. Interestingly, classical upstream (cRAF) and downstream (ERK) kinase pathways were not significantly reduced by amsulostat, pointing to a novel mechanism of PDGFR signal modulation by lysyl oxidases. ConclusionThis study provides new direct evidence that lysyl oxidase activity leads to aldehyde formation at lysine residues on the extracellular domains of growth factor receptors, including PDGFR. Such oxidations enhance overall cell surface expression after PDGF stimulation, leading to a prolonged response and augmented signaling. Importantly, these effects are blocked by amsulostat, suggesting a powerful mode of action beyond the extracellular inhibition of cross-linking

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01HL053080

  NIH · $1.0M · 1998

• NIH Grant T32HL007969

  NIH · $3.2M · 2020

• NIH Grant R01HL058547

  NIH · $1.6M · 2004

• A path to thrombosis in primary myelofibrosis

  NIH · $1.9M · 2017–2022

• NIH Grant R03AG022623

  NIH · $81k · 2005

Frequent coauthors

• Paul Toselli

  Boston University

  53 shared

• Vipul C. Chitalia

  Boston University

  43 shared

• Hao G. Nguyen

  University of California, San Francisco

  41 shared

• Carl W. Jackson

  40 shared

• Shinobu Matsuura

  University of California, San Diego

  40 shared

• Matthew R. Jones

  36 shared

• Guangyao Yu

  36 shared

• Yuka Nagata

  Toneyama National Hospital

  27 shared

Labs

• Ravid LabPI