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Molecular Mechanism in Pulmonary Embolism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 October 2026 | Viewed by 581

Special Issue Editor


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Guest Editor
Medical School, São Paulo State University (UNESP), Botucatu, SP, Brazil
Interests: pulmonary thromboembolism; pulmonary embolism; chronic pulmonary thromboembolic hypertension; thromboembolism; embolism; venous thromboembolism; pulmonary hypertension; pulmonary arterial hypertension; acute pulmonary thromboembolism

Special Issue Information

Dear Colleagues,

Pulmonary embolism (PE) remains a major cause of cardiovascular morbidity and mortality worldwide. Despite advances in diagnosis and treatment, the molecular and cellular mechanisms underlying PE pathogenesis, progression, resolution, and long-term complications remain incompletely understood. Gaining deeper mechanistic insight is essential to improve risk stratification, therapeutic strategies, and patient outcomes.

This Special Issue of the International Journal of Molecular Sciences aims to present a comprehensive and up-to-date overview of the molecular landscape of PE. We invite original research articles, authoritative reviews, and innovative perspectives exploring biological processes driving thrombogenesis, endothelial dysfunction, inflammation, coagulation, platelet activation, fibrinolysis, and vascular remodeling.

Topics of particular interest include the role of coagulation cascades, platelet activation, immune cell interactions, extracellular vesicles, and the molecular basis of PE complications. By convening leading experts and emerging investigators, this Special Issue aims to stimulate interdisciplinary dialogue and accelerate the translation of molecular insights into precision medicine approaches for improved diagnosis, risk stratification, prognosis and targeted treatment of PE.

We warmly invite the scientific community to contribute to this timely and clinically relevant collection. Submissions from diverse disciplines are welcome.

Dr. Hugo Hyung Bok Yoo
Guest Editor

Manuscript Submission Information

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Keywords

  • pulmonary embolism
  • thrombosis
  • molecular mechanisms
  • coagulation
  • endothelial dysfunction
  • biomarkers
  • inflammation
  • fibrinolysis
  • precision medicine

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Published Papers (1 paper)

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Review

24 pages, 24020 KB  
Review
Clonal Hematopoiesis (CHIP) in Pulmonary Embolism and CTEPH: Evidence, Mechanisms, and Risk Stratification
by Lukasz Szarpak, Monika E. Jach, Michal Skoczylas, Sebastian Radej and Michal Pruc
Int. J. Mol. Sci. 2026, 27(6), 2750; https://doi.org/10.3390/ijms27062750 - 18 Mar 2026
Viewed by 431
Abstract
Pulmonary embolism (PE) is biologically heterogeneous. Despite guideline-directed anticoagulation, a subset of patients develops recurrent venous thromboembolism, persistent exertional limitation, residual perfusion defects, and progression to chronic thromboembolic pulmonary disease (CTEPD) or chronic thromboembolic pulmonary hypertension (CTEPH). Conventional risk factors explain much of [...] Read more.
Pulmonary embolism (PE) is biologically heterogeneous. Despite guideline-directed anticoagulation, a subset of patients develops recurrent venous thromboembolism, persistent exertional limitation, residual perfusion defects, and progression to chronic thromboembolic pulmonary disease (CTEPD) or chronic thromboembolic pulmonary hypertension (CTEPH). Conventional risk factors explain much of the index event but incompletely account for thrombus non-resolution and chronic sequelae. Clonal hematopoiesis of indeterminate potential (CHIP)—the age-associated expansion of hematopoietic clones carrying somatic mutations—defines a measurable thrombo-inflammatory endophenotype that is strongly genotype- and clone-size (variant allele frequency; VAF)-dependent. Across human studies, JAK2-CHIP and TET2-CHIP show the most consistent associations with VTE/PE, whereas isolated DNMT3A-CHIP is frequently neutral, and larger clones tend to confer stronger effects. Mechanistically, CHIP can bias myeloid cells toward inflammasome/IL-1β signaling and endothelial activation, increase monocyte tissue factor activity, and promote immunothrombosis with neutrophil extracellular trap (NET) formation. NET-rich thrombi may adopt a dense fibrin–DNA–histone architecture that resists endogenous fibrinolysis, favoring organization and persistence. CTEPH offers a translational window to interrogate this model because thrombotic material and deep phenotyping are accessible. We synthesize genotype- and VAF-resolved clinical and mechanistic evidence using a structured strength-of-evidence framework and propose a pragmatic phenotyping roadmap with testable predictions for prospective post-PE validation. CHIP testing in PE/CTEPH remains investigational and should not currently change standard care. Full article
(This article belongs to the Special Issue Molecular Mechanism in Pulmonary Embolism)
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