Evidence map›Paper›PMID 32548548›Full record

ReviewResearch and practice in thrombosis and haemostasis2020

Plasminogen activation in the musculoskeletal acute phase response: Injury, repair, and disease.

Breanne H Y Gibson, Matthew T Duvernay, Stephanie N Moore-Lotridge, Matthew J Flick, Jonathan G Schoenecker

Open access · goldAbstract readReview
In one paragraph

Review in Research and practice in thrombosis and haemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 24% 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.

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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Large-scale circulating proteome association study (CPAS) meta-analysis identifies circulating proteins and pathways predicting incident hip fractures.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
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  14. Determining the pharmacologic window of bisphosphonates that mitigates severe injury-induced osteoporosis and muscle calcification, while preserving fracture repair.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022
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  15. Genetic heterogeneity of heritable ectopic mineralization disorders in a large international cohort.Genetics in medicine : official journal of the American College of Medical Genetics · 2022
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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

5 authors at 3 institutions in 1 country.

Breanne H Y GibsonDepartment of Pharmacology Vanderbilt University Nashville TN USA.
Matthew T DuvernayDepartment of Pharmacology Vanderbilt University Nashville TN USA.
Stephanie N Moore-LotridgeDepartment of Orthopaedics Vanderbilt University Medical Center Nashville TN USA.ORCID https://orcid.org/0000-0002-3045-4199
Matthew J FlickDepartment of Pathology and Laboratory Medicine University of North Carolina-Chapel Hill NC USA.
Jonathan G SchoeneckerDepartment of Pharmacology Vanderbilt University Nashville TN USA.ORCID https://orcid.org/0000-0002-3097-5496
Vanderbilt University · USUniversity of North Carolina at Chapel Hill · USVanderbilt University Medical Center · 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
Thrombin-dependent mechanisms of pancreatic ductal adenocarcinoma diseaseR01CA211098 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FLICK, MATTHEW J. · 2017 to 2022
$2.2M
Severe Trauma Provokes Pathologic Continuum of Plasmin ActivationR01GM126062 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SCHOENECKER, JONATHAN · 2019 to 2023
$2.0M
Fibrin(ogen) control of metabolic inflammation and obesityR01DK112778 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FLICK, MATTHEW J. · 2019 to 2022
$1.5M
The role of pathologic plasmin activity in trauma-induced systemic inflammatory response syndromeF31HL149340 · NHLBI · VANDERBILT UNIVERSITY · PI GIBSON, BREANNE HELEN YVONNE · 2019 to 2020
$60k
NCI NIH HHS R01 CA211098NHLBI NIH HHS F31 HL149340NHLBI NIH HHS U01 HL143403NIDDK NIH HHS R01 DK112778NIGMS NIH HHS R01 GM126062
6 · The paper itself

Abstract

The musculoskeletal system is critical for movement and the protection of organs. In addition to abrupt injuries, daily physical demands inflict minor injuries, necessitating a coordinated process of repair referred to as the acute-phase response (APR). Dysfunctional APRs caused by severe injuries or underlying chronic diseases are implicated in pathologic musculoskeletal repair, resulting in decreased mobility and chronic pain. The molecular mechanisms behind these phenomena are not well understood, hindering the development of clinical solutions. Recent studies indicate that, in addition to regulating intravascular clotting, the coagulation and fibrinolytic systems are also entrenched in tissue repair. Although plasmin and fibrin are considered antithetical to one another in the context of hemostasis, in a proper APR, they complement one another within a coordinated spatiotemporal framework. Once a wound is contained by fibrin, activation of plasmin promotes the removal of fibrin and stimulates angiogenesis, tissue remodeling, and tissue regeneration. Insufficient fibrin deposition or excessive plasmin-mediated fibrinolysis in early convalescence prevents injury containment, causing bleeding. Alternatively, excess fibrin deposition and/or inefficient plasmin activity later in convalescence impairs musculoskeletal repair, resulting in tissue fibrosis and osteoporosis, while inappropriate fibrin or plasmin activity in a synovial joint can cause arthritis. Together, these pathologic conditions lead to chronic pain, poor mobility, and diminished quality of life. In this review, we discuss both fibrin-dependent and -independent roles of plasminogen activation in the musculoskeletal APR, how dysregulation of these mechanisms promote musculoskeletal degeneration, and the possibility of therapeutically manipulating plasmin or fibrin to treat musculoskeletal disease.

Indexed as

acute‐phase reactionfibrinogenmusculoskeletal diseasesplasminogenplasminogen activatorsrheumatic diseases

Identifiers

PMID32548548
PMCPMC7293893
OpenAlexW3035421593

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.