ReviewFrontiers in immunology2019
Plasminflammation-An Emerging Pathway to Bradykinin Production.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Clinical features of genetically characterized types of hereditary angioedema with normal C1 inhibitor: a systematic review of qualitative evidence.Orphanet journal of rare diseases · 2020Pooled it
- Modulation of immune responses by opioids through toll-like and P2X receptor signaling in COVID-19.Purinergic signalling · 2026Review
- Therapeutic Advances in Hereditary Angioedema: A Focus on Present and Future Options.Advances in therapy · 2025Review
- Review
- Aprotinin (I): Understanding the Role of Host Proteases in COVID-19 and the Importance of Pharmacologically Regulating Their Function.International journal of molecular sciences · 2024Review
- Aprotinin (II): Inhalational Administration for the Treatment of COVID-19 and Other Viral Conditions.International journal of molecular sciences · 2024Review
- A mechanism for hereditary angioedema caused by a methionine-379-to-lysine substitution in kininogens.Blood · 2024Article
- Plasminogen missense variants and their involvement in cardiovascular and inflammatory disease.Frontiers in cardiovascular medicine · 2024Review
- Tranexamic acid for haemostasis and beyond: does dose matter?Thrombosis journal · 2023Review
- Mechanisms involved in hereditary angioedema with normal C1-inhibitor activity.Frontiers in physiology · 2023Review
- "Super" SERPINs-A stabilizing force against fibrinolysis in thromboinflammatory conditions.Frontiers in cardiovascular medicine · 2023Review
- Variable Response to Antifibrinolytics Correlates with Blood-loss and Transfusion in Posterior Spinal Fusion.Spine deformity · 2022Article
- A mechanism for hereditary angioedema caused by a lysine 311-to-glutamic acid substitution in plasminogen.Blood · 2022Article
- Review
- Plasma Kallikrein Cleaved H-kininogen: An End-Point Marker for Contact ActivationFrontiers in cardiovascular medicine · 2022Article
- How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment.Frontiers in immunology · 2022Review
- Plasmin drives burn-induced systemic inflammatory response syndrome.JCI insight · 2021Article
- Nrf2 activator PB125® as a carnosic acid-based therapeutic agent against respiratory viral diseases, including COVID-19.Free radical biology & medicine · 2021Review
- Renin-Angiotensin System in Pathogenesis of Atherosclerosis and Treatment of CVD.International journal of molecular sciences · 2021Review
- The Fibrinolytic System: Mysteries and Opportunities.HemaSphere · 2021Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasminogen activation is essential for fibrinolysis-the breakdown of fibrin polymers in blood clots. Besides this important function, plasminogen activation participates in a wide variety of inflammatory conditions. One of these conditions is hereditary angioedema (HAE), a rare disease with characteristic attacks of aggressive tissue swelling due to unregulated production and activity of the inflammatory mediator bradykinin. Plasmin was already implicated in this disease decades ago, but a series of recent discoveries have made it clear that plasmin actively contributes to this pathology. Collective evidence points toward an axis in which the plasminogen activation system and the contact system (which produces bradykinin) are mechanistically coupled. This is amongst others supported by findings in subtypes of HAE that are caused by gain-of-function mutations in the genes that respectively encode factor XII or plasminogen, as well as clinical experience with the antifibrinolytic agents in HAE. The concept of a link between plasminogen activation and the contact system helps us to explain the inflammatory side effects of fibrinolytic therapy, presenting as angioedema or tissue edema. Furthermore, these observations motivate the development and characterization of therapeutic agents that disconnect plasminogen activation from bradykinin production.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.