Evidence map›Paper›PMID 30235807›Full record

ReviewDiseases (Basel, Switzerland)2018

Emerging Therapeutic Targets and Experimental Drugs for the Treatment of NAFLD.

Pratima Dibba, Andrew A Li, Brandon J Perumpail, Nimy John, Sandy Sallam, Neha D Shah, Waiyee Kwong, George Cholankeril, Donghee Kim, Aijaz Ahmed

Open access · goldAbstract readReview
In one paragraph

Review in Diseases (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Therapeutic Effect of Crocin on the NASH Model by Targeting the Fas Receptor Signaling Pathway.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. 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

10 authors at 3 institutions in 1 country.

Pratima DibbaDivision of Gastroenterology, Women & Infants Hospital/Warren Alpert School of Medicine, Brown University, Providence, RI 02905, USA. pratima_dibba@brown.edu.ORCID 0000-0002-3979-7200
Andrew A LiDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94304, USA. andrewli@stanford.edu.
Brandon J PerumpailDrexel University College of Medicine, Philadelphia, PA 19129, USA. brandonperumpail@gmail.com.
Nimy JohnDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. nionnj@gmail.com.
Sandy SallamDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. SSallam@stanfordhealthcare.org.
Neha D ShahDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. NeShah@stanfordhealthcare.org.
Waiyee KwongDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. WKwong@stanfordhealthcare.org.
George CholankerilDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. georgetc@stanford.edu.
Donghee KimDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. dhkimmd@stanford.edu.ORCID 0000-0003-1919-6800
Aijaz AhmedDivision of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94304, USA. aijazahmed@stanford.edu.ORCID 0000-0002-3609-8586
Stanford University · USBrown University · USDrexel University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The two main subsets of nonalcoholic fatty liver disease (NAFLD) include: (1) nonalcoholic fatty liver (NAFL), the more common and non-progressive subtype; and (2) nonalcoholic steatohepatitis (NASH), the less common subtype, which has the potential to progress to advanced liver damage. Current treatment strategies have focused on lifestyle management of modifiable risk factors, namely weight, and on the optimization of the management of individual components of metabolic syndrome. Various hypothetical pathogenic mechanisms have been proposed, leading to the development of novel drugs with the potential to effectively treat patients with NASH. Numerous clinical trials are ongoing, utilizing these experimental drugs and molecules targeting specific mechanistic pathway(s) to effectively treat NASH. Some of these mechanistic pathways targeted by experimental pharmacologic agents include chemokine receptor 2 and 5 antagonism, inhibition of galectin-3 protein, antagonism of toll-like receptor 4, variation of fibroblast growth factor 19, agonism of selective thyroid hormone receptor-beta, inhibition of apoptosis signal-regulating kinase 1, inhibition of acetyl-coenzyme A carboxylase, agonism of farnesoid X receptor, antibodies against lysl oxidase-like-2, and inhibition of inflammasomes. Emerging data are promising and further updates from ongoing clinical trials are eagerly awaited.

Indexed as

acetyl-coenzyme A carboxylaseapoptosis signal-regulating kinase 1chemokine receptor 2 and 5drug therapyfarnesoid X receptorfibroblast growth factor 19galectin-3 proteininflammasomesNAFLDNASHnonalcoholic fatty liver diseaseselective thyroid hormone receptor-betatoll-like receptor 4

Identifiers

PMID30235807
PMCPMC6164020
OpenAlexW2891680487

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.