Evidence map›Paper›PMID 31261968›Full record

ReviewCells2019

The Lymphatic Headmaster of the Mast Cell-Related Splanchnic Inflammation in Portal Hypertension.

Maria-Angeles Aller, Javier Blanco-Rivero, Natalia Arias, Luis Santamaria, Jaime Arias

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact, top 88% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Trial
  2. Review
  3. Impact of High-Temperature Feeds on Gut Microbiota and MAFLD.Journal of microbiology and biotechnology · 2024
    Article
  4. 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

5 authors at 4 institutions in 2 countries.

Maria-Angeles AllerDepartment of Surgery, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain. maaller@ucm.es.
Javier Blanco-RiveroDepartment of Physiology, School of Medicine, Autonomous University of Madrid, 28049 Madrid, Spain.
Natalia AriasDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London WC2R 2LS, UK.
Luis SantamariaDepartment of Anatomy, Histology and Neuroscience, School of Medicine, Autonoma University of Madrid, 28029 Madrid, Spain.
Jaime AriasDepartment of Surgery, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain.
Universidad Complutense de Madrid · ESCentro de Investigación Biomédica en Red · ESKing's College London · GBUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Portal hypertension is a common complication of liver disease, either acute or chronic. Consequently, in chronic liver disease, such as the hypertensive mesenteric venous pathology, the coexisting inflammatory response is classically characterized by the splanchnic blood circulation. However, a vascular lymphatic pathology is produced simultaneously with the splanchnic arterio-venous impairments. The pathological increase of the mesenteric venous pressure, by mechanotransduction of the venous endothelium hyperpressure, causes an inflammatory response involving the subendothelial mast cells and the lymphatic endothelium of the intestinal villi lacteal. In portal hypertension, the intestinal lymphatic inflammatory response through the development of mesenteric-systemic lymphatic collateral vessels favors the systemic diffusion of substances with a molecular pattern associated with damage and pathogens of intestinal origin. When the chronic hepatic insufficiency worsens the portal hypertensive inflammatory response, the splanchnic lymphatic system transports the hyperplasied intestinal mast cells to the mesenteric lymphatic complex. Then, an acquired immune response regulating a new hepato-intestinal metabolic scenario is activated. Therefore, reduction of the hepatic metabolism would reduce its key centralized functions, such as the metabolic, detoxifying and antioxidant functions which would try to be substituted by their peroxisome activity, among other functions of the mast cells.

Indexed as

HumansHypertension, PortalInflammationIntestinal MucosaLymphatic VesselsMast CellsMechanotransduction, CellularMesenteric VeinsMesenterySplanchnic Circulationlymphaticsmast cellsperoxisomesportal hypertension

Identifiers

PMID31261968
PMCPMC6678304
OpenAlexW2956122989

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.