Evidence map›Paper›PMID 35893744›Full record

ReviewPharmaceuticals (Basel, Switzerland)2022

Matrix Metalloproteinase 2 as a Pharmacological Target in Heart Failure.

Pricila Rodrigues Gonçalves, Lisandra Duarte Nascimento, Raquel Fernanda Gerlach, Keuri Eleutério Rodrigues, Alejandro Ferraz Prado

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Vascular Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2024
    Review
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 2 institutions in 1 country.

Pricila Rodrigues GonçalvesCardiovascular System Pharmacology and Toxicology Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, PA, Brazil.
Lisandra Duarte NascimentoCardiovascular System Pharmacology and Toxicology Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, PA, Brazil.
Raquel Fernanda GerlachDepartment of Basic and Oral Biology, Faculty of Dentistry of Ribeirao Preto, University of Sao Paulo (FORP/USP), Ribeirao Preto 14040-904, SP, Brazil.
Keuri Eleutério RodriguesCardiovascular System Pharmacology and Toxicology Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, PA, Brazil.
Alejandro Ferraz PradoCardiovascular System Pharmacology and Toxicology Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, PA, Brazil.ORCID 0000-0001-7495-9837
Universidade Federal do Pará · BRUniversidade de Ribeirão Preto · BR

Funding

Conselho Nacional de Desenvolvimento científico e Tecnológico (CNPq) 427591/2018-0Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brasil (CAPES) 001São Paulo Research Foundation 2014-23888-0
6 · The paper itself

Abstract

Heart failure (HF) is an acute or chronic clinical syndrome that results in a decrease in cardiac output and an increase in intracardiac pressure at rest or upon exertion. The pathophysiology of HF is heterogeneous and results from an initial harmful event in the heart that promotes neurohormonal changes such as autonomic dysfunction and activation of the renin-angiotensin-aldosterone system, endothelial dysfunction, and inflammation. Cardiac remodeling occurs, which is associated with degradation and disorganized synthesis of extracellular matrix (ECM) components that are controlled by ECM metalloproteinases (MMPs). MMP-2 is part of this group of proteases, which are classified as gelatinases and are constituents of the heart. MMP-2 is considered a biomarker of patients with HF with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF). The role of MMP-2 in the development of cardiac injury and dysfunction has clearly been demonstrated in animal models of cardiac ischemia, transgenic models that overexpress MMP-2, and knockout models for this protease. New research to minimize cardiac structural and functional alterations using non-selective and selective inhibitors for MMP-2 demonstrates that this protease could be used as a possible pharmacological target in the treatment of HF.

Indexed as

cardiac dysfunctionischemiaMMP-2 inhibitor

Identifiers

PMID35893744
PMCPMC9331741
OpenAlexW4287878589

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.