Evidence map›Paper›PMID 27012771›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2016

Lin28 and let-7: roles and regulation in liver diseases.

Kelly McDaniel, Chad Hall, Keisaku Sato, Terry Lairmore, Marco Marzioni, Shannon Glaser, Fanyin Meng, Gianfranco Alpini

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Association ofBiomedicines · 2024
    Article
  3. Article
  4. Review
  5. Increased let-7d-5p in non-alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis.Liver international : official journal of the International Association for the Study of the Liver · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 4 institutions in 2 countries.

Kelly McDanielResearch, Central Texas Veterans Health Care System, Temple, Texas; Baylor Scott & White Digestive Disease Research Center, Scott & White Memorial Hospital, Temple, Texas; Operational Funds, Baylor Scott & White, Temple, Texas; Department of Medicine, Baylor Scott & White and Texas A & M Health Science Center, Temple, Texas;
Chad HallOperational Funds, Baylor Scott & White, Temple, Texas; Department of Surgery, Baylor Scott & White and Texas A & M Health Science Center, Temple, Texas; and.
Keisaku SatoDepartment of Medicine, Baylor Scott & White and Texas A & M Health Science Center, Temple, Texas;
Terry LairmoreOperational Funds, Baylor Scott & White, Temple, Texas; Department of Surgery, Baylor Scott & White and Texas A & M Health Science Center, Temple, Texas; and.
Marco MarzioniDepartment of Medicine, Universita' Politecnica delle Marche, Ancona, Italy.
Shannon GlaserResearch, Central Texas Veterans Health Care System, Temple, Texas; Baylor Scott & White Digestive Disease Research Center, Scott & White Memorial Hospital, Temple, Texas; Operational Funds, Baylor Scott & White, Temple, Texas;
Fanyin MengResearch, Central Texas Veterans Health Care System, Temple, Texas; Baylor Scott & White Digestive Disease Research Center, Scott & White Memorial Hospital, Temple, Texas; Operational Funds, Baylor Scott & White, Temple, Texas;
Gianfranco AlpiniResearch, Central Texas Veterans Health Care System, Temple, Texas; Baylor Scott & White Digestive Disease Research Center, Scott & White Memorial Hospital, Temple, Texas; Department of Medicine, Baylor Scott & White and Texas A & M Health Science Center, Temple, Texas; galpini@tamu.edu.
Baylor Scott & White Medical Center - Temple · USCentral Texas Veterans Health Care System · USMarche Polytechnic University · ITScott & White Memorial Hospital · US

Funding

GROWTH REGULATION OF THE INTRAHEPATIC BILIARY TREER01DK054811 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI ALPINI, GIANFRANCO D, GLASER, SHANNON STROUD · 2000 to 2021
$3.8M
Role of Sensory Neuropeptides in the Regulation of Biliary FunctionR01DK076898 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI ALPINI, GIANFRANCO D, GLASER, SHANNON STROUD · 2008 to 2016
$1.8M
TOWARD THE OPTIMAL TIMING OF INITIATION OF DIALYSISR01DK058411 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHERTOW, GLENN MATTHEW · 2001 to 2003
$1.8M
The Role of Stem Cell Derived Microvesicles in Cholestatic Liver InjuryR01DK107310 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI ALPINI, GIANFRANCO D, GLASER, SHANNON STROUD · 2015 to 2019
$1.7M
Functional characters of non-coding RNAs in alcoholic liver injuryI01BX001724 · VA · RLR VA MEDICAL CENTER · PI MENG, FANYIN · 2012 to 2024
–
Role of Mechanosensitive Receptors During Biliary Proliferation and FibrosisI01BX002192 · VA · OLIN TEAGUE VETERANS CENTER · PI GLASER, SHANNON STROUD · 2014 to 2018
–
Autocrine/Paracrine Regulation of Intrahepatic Bile Duct GrowthI01BX000574 · VA · RLR VA MEDICAL CENTER · PI ALPINI, GIANFRANCO D · 2009 to 2022
–
BLRD VA I01 BX000574BLRD VA I01 BX001724BLRD VA I01 BX002192NIDDK NIH HHS R01 DK054811NIDDK NIH HHS R01 DK058411NIDDK NIH HHS R01 DK076898NIDDK NIH HHS R01 DK107310
6 · The paper itself

Abstract

The diagnosis and treatment of liver disease remain a major health concern worldwide because of the diverse etiologies of this disease. For this reason, new therapeutic targets are greatly needed to halt the progression of this damaging disease. Upon initiation of liver injury by viral infection, autoimmune disease or toxin, and/or hepatitis, chronic disease may develop, which can progress to cirrhosis, hepatocellular carcinoma (HCC), cholangiocarcinoma, liver failure, or death. The Lin28/lethal-7 (let-7) molecular switch has emerged as a central regulator of multiorgan injuries and cancer development. Lin28 is a stem cell marker vital to initiation or maintenance of a stem cell phenotype. Lin28 has not been extensively studied in the liver, despite its ability to induce tissue regeneration via reprogramming of oxidative enzymes in other tissues and its involvement with numerous upstream regulators and downstream targets in liver disease. Theoretically, overexpression of Lin28 in certain forms of liver disease could be a potential treatment that aids in liver regeneration. Alternatively, Lin28 has been implicated numerous times in the progression of diverse cancer types and is associated with increased severity of disease. In this case, Lin28 could be a potential inhibitory target to prevent malignant transformation in the liver. This review seeks to characterize the role of Lin28 in liver disease.

Indexed as

AnimalsCell CycleHumansLiver DiseasesLiver RegenerationMicroRNAsRNA-Binding ProteinsSignal TransductionLin28A protein, humanMicroRNAsmirnlet7 microRNA, humanRNA-Binding Proteinshepatic disordershepatocellular carcinomalethal-7liver diseaseliver repairprimary biliary cholangitisprimary sclerosing cholangitis

Identifiers

PMID27012771
PMCPMC4888551
OpenAlexW2303901593

What OpenQuestion holds

Textmetadata
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.