Evidence map›Paper›PMID 34924021›Full record

ReviewExperimental hematology & oncology2021

Role of the lectin pathway of complement in hematopoietic stem cell transplantation-associated endothelial injury and thrombotic microangiopathy.

Eleni Gavriilaki, Vincent T Ho, Wilhelm Schwaeble, Thomas Dudler, Mohamed Daha, Teizo Fujita, Sonata Jodele

Abstract readReview
In one paragraph

Review in Experimental hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

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  17. High-dose systemic adeno-associated virus vector administration causes liver and sinusoidal endothelial cell injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Eleni GavriilakiHematology Department-BMT Unit, G Papanikolaou Hospital, Leof. Papanikolaou, Pilea Chortiatis 570 10, Thessaloniki, Greece. elenicelli@yahoo.gr.ORCID http://orcid.org/0000-0002-8883-8208
Vincent T HoDepartment of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Ave, Boston, MA, 02215, USA.
Wilhelm SchwaebleDepartment of Veterinary Medicine, University of Cambridge, Cambridge, CB3 0ES, UK.
Thomas DudlerDiscovery and Development, Omeros Corporation, 201 Elliott Ave W, Seattle, WA, 98119, USA.
Mohamed DahaDepartment of Nephrology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, Netherlands.
Teizo FujitaDepartment Fukushima Prefectural General Hygiene Institute, 61-Watari-Nakakado, Fukushima, Fukushima, 960-8141, Japan.
Sonata JodeleDivision of Bone Marrow Transplantation and Immune Deficiency, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH, 45229, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy (HSCT-TMA) is a life-threatening syndrome that occurs in adult and pediatric patients after hematopoietic stem cell transplantation. Nonspecific symptoms, heterogeneity within study populations, and variability among current diagnostic criteria contribute to misdiagnosis and underdiagnosis of this syndrome. Hematopoietic stem cell transplantation and associated risk factors precipitate endothelial injury, leading to HSCT-TMA and other endothelial injury syndromes such as hepatic veno-occlusive disease/sinusoidal obstruction syndrome, idiopathic pneumonia syndrome, diffuse alveolar hemorrhage, capillary leak syndrome, and graft-versus-host disease. Endothelial injury can trigger activation of the complement system, promoting inflammation and the development of endothelial injury syndromes, ultimately leading to organ damage and failure. In particular, the lectin pathway of complement is activated by damage-associated molecular patterns (DAMPs) on the surface of injured endothelial cells. Pattern-recognition molecules such as mannose-binding lectin (MBL), collectins, and ficolins-collectively termed lectins-bind to DAMPs on injured host cells, forming activation complexes with MBL-associated serine proteases 1, 2, and 3 (MASP-1, MASP-2, and MASP-3). Activation of the lectin pathway may also trigger the coagulation cascade via MASP-2 cleavage of prothrombin to thrombin. Together, activation of complement and the coagulation cascade lead to a procoagulant state that may result in development of HSCT-TMA. Several complement inhibitors targeting various complement pathways are in clinical trials for the treatment of HSCT-TMA. In this article, we review the role of the complement system in HSCT-TMA pathogenesis, with a focus on the lectin pathway.

Indexed as

Complement activationEndothelial injuryHematopoietic stem cell transplantation-associated thrombotic microangiopathyLectin pathway

Identifiers

PMID34924021
PMCPMC8684592

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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.