ArticleNature communications2022
MARTX toxin of Vibrio vulnificus induces RBC phosphatidylserine exposure that can contribute to thrombosis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- RTX-family toxin EhxA drives morphological remodeling and thrombogenesis in RBCs during enterohemorrhagicScience advances · 2026Article
- It's time to act: Understanding and combatingVirulence · 2025Review
- Red Blood Cell-Associated Features of Adenoviral Vector-Linked Venous Thrombosis.International journal of molecular sciences · 2025Article
- Exogenous phosphatidylserine protects against mesenteric ischemia-reperfusion with associated Akt/mTOR pathway upregulation.Scientific reports · 2025Article
- TolCV1 inhibition by NPPB rendersAntimicrobial agents and chemotherapy · 2025Article
- Genome-wide phenotypic profiling of transcription factors and identification of novel targets to control the virulence of Vibrio vulnificus.Nucleic acids research · 2025Article
- Vibrio vulnificus Bacteremia With Compartment Syndrome: A Case Report and Characterization of the Isolate.Cureus · 2024Article
- Structural basis of the activation of MARTX cysteine protease domain from Vibrio vulnificus.PloS one · 2024Article
- Crucial roles of red blood cells and platelets in whole blood thrombin generation.Blood advances · 2023Article
- An Overview of Clinical Manifestations of Dermatological Disorders in Intensive Care Units: What Should Intensivists Be Aware of?Diagnostics (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
V. vulnificus-infected patients suffer from hemolytic anemia and circulatory lesions, often accompanied by venous thrombosis. However, the pathophysiological mechanism of venous thrombosis associated with V. vulnificus infection remains largely unknown. Herein, V. vulnificus infection at the sub-hemolytic level induced shape change of human red blood cells (RBCs) accompanied by phosphatidylserine exposure, and microvesicle generation, leading to the procoagulant activation of RBCs and ultimately, acquisition of prothrombotic activity. Of note, V. vulnificus exposed to RBCs substantially upregulated the rtxA gene encoding multifunctional autoprocessing repeats-in-toxin (MARTX) toxin. Mutant studies showed that V. vulnificus-induced RBC procoagulant activity was due to the pore forming region of the MARTX toxin causing intracellular Ca
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