Evidence map›Paper›PMID 30523120›Full record

ReviewBlood2019

The multifaceted role of fibrinogen in tissue injury and inflammation.

James P Luyendyk, Jonathan G Schoenecker, Matthew J Flick

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05691985 (Fibrinogen to Albumin Ratio), which is not on this map. Cited by 328 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
328citing papers in PubMed, 1 pooled it
28.4field-weighted citation impact, top 1% of its field
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.

NCT05691985 unknown statusnot on this mapstarted 2024, after this paper: background citation

Fibrinogen to Albumin Ratio (FAR) as a Risk Factor for Type 2 Diabetic Nephropathy(DN)

Typeobservational_patient_registrySponsorAssiut UniversityRan2024 to 2025Enrolled50ConditionsCKD, Type 2 Diabetes
3 · Its place in the literature

Who cites it

328 citing papers in PubMed, 1 synthesis or guideline pooled it, 549 citations in OpenAlex.

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268 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

James P LuyendykDepartment of Pathobiology and Diagnostic Investigation.ORCID 0000-0003-3174-8583
Jonathan G SchoeneckerDepartment of Orthopaedics.
Matthew J FlickDivision of Experimental Hematology and Cancer Biology, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Cincinnati Children's Hospital Medical Center · USMichigan State University · USPediatrics and Genetics · US

Funding

Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated ThrombosisU01HL143403 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FISHEL, MELISSA L., FLICK, MATTHEW J. · 2018 to 2022
$4.2M
Novel anti-fibrotic mechanisms in chemical-induced liver injuryR01ES017537 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUYENDYK, JAMES P · 2009 to 2019
$3.6M
Thrombin-dependent mechanisms of pancreatic ductal adenocarcinoma diseaseR01CA211098 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FLICK, MATTHEW J. · 2017 to 2022
$2.2M
Novel mechanisms stimulating liver repair after acetaminophen overdoseR01DK105099 · NIDDK · MICHIGAN STATE UNIVERSITY · PI LUYENDYK, JAMES P · 2015 to 2018
$1.4M
NCI NIH HHS R01 CA211098NHLBI NIH HHS U01 HL143403NIDDK NIH HHS R01 DK105099NIEHS NIH HHS R01 ES017537
6 · The paper itself

Abstract

The canonical role of the hemostatic and fibrinolytic systems is to maintain vascular integrity. Perturbations in either system can prompt primary pathological end points of hemorrhage or thrombosis with vessel occlusion. However, fibrin(ogen) and proteases controlling its deposition and clearance, including (pro)thrombin and plasmin(ogen), have powerful roles in driving acute and reparative inflammatory pathways that affect the spectrum of tissue injury, remodeling, and repair. Indeed, fibrin(ogen) deposits are a near-universal feature of tissue injury, regardless of the nature of the inciting event, including injuries driven by mechanical insult, infection, or immunological derangements. Fibrin can modify multiple aspects of inflammatory cell function by engaging leukocytes through a variety of cellular receptors and mechanisms. Studies on the role of coagulation system activation and fibrin(ogen) deposition in models of inflammatory disease and tissue injury have revealed points of commonality, as well as context-dependent contributions of coagulation and fibrinolytic factors. However, there remains a critical need to define the precise temporal and spatial mechanisms by which fibrinogen-directed inflammatory events may dictate the severity of tissue injury and coordinate the remodeling and repair events essential to restore normal organ function. Current research trends suggest that future studies will give way to the identification of novel hemostatic factor-targeted therapies for a range of tissue injuries and disease.

Indexed as

AnimalsFibrinogenHumansInflammationWounds and InjuriesFibrinogen

Identifiers

PMID30523120
PMCPMC6367649
OpenAlexW2903302497

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.