Evidence map›Paper›PMID 32355844›Full record

ReviewAnnals of translational medicine2020

The cellular pathways of liver fibrosis in non-alcoholic steatohepatitis.

Nahum Méndez-Sánchez, Alejandro Valencia-Rodríguez, Carlos Coronel-Castillo, Alfonso Vera-Barajas, Jocelyn Contreras-Carmona, Guadalupe Ponciano-Rodríguez, Daniel Zamora-Valdés

Open access · diamondAbstract readReview
In one paragraph

Review in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 49 citations in OpenAlex.

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  11. The Role of CD4International journal of molecular sciences · 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 at 2 institutions in 1 country.

Nahum Méndez-SánchezLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Alejandro Valencia-RodríguezLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Carlos Coronel-CastilloLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Alfonso Vera-BarajasLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Jocelyn Contreras-CarmonaLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Guadalupe Ponciano-RodríguezPublic Health Department, Faculty of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.
Daniel Zamora-ValdésLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Hospital Médica Sur · MXUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic steatohepatitis (NASH) is considered the advanced stage of non-alcoholic fatty liver disease (NAFLD). It is characterized by liver steatosis, inflammation and different degrees of fibrosis. Although the exact mechanisms by which fatty liver progresses to NASH are still not well understood, innate and adaptive immune responses seem to be essential key regulators in the establishment, progression, and chronicity of these disease. Diet-induced lipid overload of parenchymal and non-parenchymal liver cells is considered the first step for the development of fatty liver with the consequent organelle dysfunction, cellular stress and liver injury. These will generate the production of pro-inflammatory cytokines, chemokines and damage-associated molecular patterns (DAMPs) that will upregulate the activation of Kupffer cells (KCs) and monocyte-derived macrophages (MMs) favoring the polarization of the tolerogenic environment of the liver to an immunogenic phenotype with the resulting transdifferentiation of hepatic stellate cells (HSCs) into myofibroblasts developing fibrosis. In the long run, dendritic cells (DCs) will activate CD4+ T cells polarizing into the pro-inflammatory lymphocytes Th1 and Th17 worsening the liver damage and inflammation. Therefore, the objective of this review is to discuss in a systematic way the mechanisms known so far of the immune and non-proper immune liver cells in the development and progression of NASH.

Indexed as

Immune systemliver cellsliver fibrosisnon-alcoholic steatohepatitis (NASH)

Identifiers

PMID32355844
PMCPMC7186641
OpenAlexW3011968644

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.