Evidence map›Paper›PMID 34066088›Full record

ArticleInternational journal of molecular sciences2021

Alternative C3 Complement System: Lipids and Atherosclerosis.

Maisa Garcia-Arguinzonis, Elisa Diaz-Riera, Esther Peña, Rafael Escate, Oriol Juan-Babot, Pedro Mata, Lina Badimon, Teresa Padro

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  9. Roles of Single Nucleotide Polymorphisms ofReviews in cardiovascular medicine · 2024
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  15. Review
  16. Molecular Research in Cardiovascular Disease.International journal of molecular sciences · 2021
    Article
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

8 authors at 2 institutions in 1 country.

Maisa Garcia-ArguinzonisCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.
Elisa Diaz-RieraCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.ORCID 0000-0002-6211-4877
Esther PeñaCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.ORCID 0000-0003-2750-0614
Rafael EscateCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.
Oriol Juan-BabotCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.
Pedro MataFundación Hipercolesterolemia Familiar, 28010 Madrid, Spain.
Lina BadimonCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.ORCID 0000-0002-9162-2459
Teresa PadroCardiovascular Program-ICCC, Research Institute-Hospital Santa Creu i Sant Pau, IIB-Sant Pau, 08025 Barcelona, Spain.ORCID 0000-0003-1921-954X
Instituto de Salud Carlos III · ESHospital de Sant Pau · ES

Funding

STUDY OF ULTRASONICALLY INDUCED OCULAR DAMAGER01EY001480 · NEI · RIVERSIDE RESEARCH INSTITUTE · PI FELEPPA, ERNEST JOSEPH · 1985 to 1990
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Instituto de Salud Carlos III CIBERCVInstituto de Salud Carlos III PI19/01687Instituto de Salud Carlos III RD16/0011/0018Secretaria d'Universitats i Recerca del Departament d'Empresa i Coneixement de la Generalitat de Catalunya 2017 SGR 1480Spanish Ministry of Economy and Competitiveness of Science PID2019-107160RB-I00
6 · The paper itself

Abstract

Familial hypercholesterolemia (FH) is increasingly associated with inflammation, a phenotype that persists despite treatment with lipid lowering therapies. The alternative C3 complement system (C3), as a key inflammatory mediator, seems to be involved in the atherosclerotic process; however, the relationship between C3 and lipids during plaque progression remains unknown. The aim of the study was to investigate by a systems biology approach the role of C3 in relation to lipoprotein levels during atherosclerosis (AT) progression and to gain a better understanding on the effects of C3 products on the phenotype and function of human lipid-loaded vascular smooth muscle cells (VSMCs). By mass spectrometry and differential proteomics, we found the extracellular matrix (ECM) of human aortas to be enriched in active components of the C3 complement system, with a significantly different proteomic signature in AT segments. Thus, C3 products were more abundant in AT-ECM than in macroscopically normal segments. Furthermore, circulating C3 levels were significantly elevated in FH patients with subclinical coronary AT, evidenced by computed tomographic angiography. However, no correlation was identified between circulating C3 levels and the increase in plaque burden, indicating a local regulation of the C3 in AT arteries. In cell culture studies of human VSMCs, we evidenced the expression of C3, C3aR (anaphylatoxin receptor) and the integrin α

Indexed as

AdultAtherosclerosisCase-Control StudiesCell AdhesionCells, CulturedComplement C3FemaleHumansHyperlipoproteinemia Type IIMaleMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleProteomeVascular RemodelingWound HealingComplement C3Proteomeatherosclerosiscardiovascular diseasecomplement systemmass spectrometryproteomics

Identifiers

PMID34066088
PMCPMC8151937
OpenAlexW3162741814

What OpenQuestion 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 OpenQuestion graph.