Evidence map›Paper›PMID 36894027›Full record

ReviewPharmacology & therapeutics2023

Endotheliopathy in the metabolic syndrome: Mechanisms and clinical implications.

Kunimaro Furuta, Xiaofang Tang, Shahidul Islam, Alonso Tapia, Zhen Bouman Chen, Samar H Ibrahim

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  11. miR-92a aggravates metabolic syndrome via KLF2/miR-483 axis.Journal of diabetes investigation · 2025
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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

6 authors at 2 institutions in 2 countries.

Kunimaro FurutaDivision of Gastroenterology & Hepatology, Mayo Clinic, Rochester, MN, USA; Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Xiaofang TangDepartment of Diabetes Complications & Metabolism, City of Hope Comprehensive Cancer Center, Duarte, CA, USA.
Shahidul IslamDivision of Gastroenterology & Hepatology, Mayo Clinic, Rochester, MN, USA.
Alonso TapiaDepartment of Diabetes Complications & Metabolism, City of Hope Comprehensive Cancer Center, Duarte, CA, USA.
Zhen Bouman ChenDepartment of Diabetes Complications & Metabolism, City of Hope Comprehensive Cancer Center, Duarte, CA, USA. Electronic address: zhenchen@coh.org.
Samar H IbrahimDivision of Gastroenterology & Hepatology, Mayo Clinic, Rochester, MN, USA; Division of Pediatric Gastroenterology & Hepatology, Mayo Clinic, Rochester, MN, USA. Electronic address: ibrahim.samar@mayo.edu.
City of Hope · USMayo Clinic in Arizona · US

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Samar Ibrahim · 2009 to 2026
$22.2M
Lipotoxicity and Liver InflammationR01DK122948 · NIDDK · MAYO CLINIC ROCHESTER · PI Samar Ibrahim · 2020 to 2026
$3.1M
Long non-coding RNA-mediated chromatin remodeling in angiogenesisR01HL145170 · NHLBI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHEN, ZHEN BOUMAN · 2019 to 2023
$2.6M
NHLBI NIH HHS R01 HL145170NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK122948
6 · The paper itself

Abstract

The increasing prevalence of the metabolic syndrome (MetS) is a threat to global public health due to its lethal complications. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the MetS characterized by hepatic steatosis, which is potentially progressive to the inflammatory and fibrotic nonalcoholic steatohepatitis (NASH). The adipose tissue (AT) is also a major metabolic organ responsible for the regulation of whole-body energy homeostasis, and thereby highly involved in the pathogenesis of the MetS. Recent studies suggest that endothelial cells (ECs) in the liver and AT are not just inert conduits but also crucial mediators in various biological processes via the interaction with other cell types in the microenvironment both under physiological and pathological conditions. Herein, we highlight the current knowledge of the role of the specialized liver sinusoidal endothelial cells (LSECs) in NAFLD pathophysiology. Next, we discuss the processes through which AT EC dysfunction leads to MetS progression, with a focus on inflammation and angiogenesis in the AT as well as on endothelial-to-mesenchymal transition of AT-ECs. In addition, we touch upon the function of ECs residing in other metabolic organs including the pancreatic islet and the gut, the dysregulation of which may also contribute to the MetS. Finally, we highlight potential EC-based therapeutic targets for human MetS, and NASH based on recent achievements in basic and clinical research and discuss how to approach unsolved problems in the field.

Indexed as

Metabolic SyndromeNon-alcoholic Fatty Liver DiseaseEndothelial CellsHumansLiverLiver CirrhosisAdipose tissue (AT)CapillarizationEndothelial cell (EC)Endothelial-to-mesenchymal transition (EndoMT)EndotheliopathyFibrosisInflammationLiver sinusoidal endothelial cell (LSEC)Metabolic syndrome (MetS)Nonalcoholic fatty liver disease (NAFLD)Nonalcoholic steatohepatitis (NASH)

Identifiers

PMID36894027
PMCPMC10084912
OpenAlexW4323353100

What OpenQuestion holds

Textmetadata
LicenceTDM
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.