Evidence map›Paper›PMID 35038955›Full record

ArticleBioengineered2022

MicroRNA-665-3p exacerbates nonalcoholic fatty liver disease in mice.

Yuanjie Yu, Tian Tian, Shiyun Tan, Pengbo Wu, Yitian Guo, Ming Li, Mengjun Huang

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Hepatic medicine : evidence and research · 2024
    Article
  12. Review
  13. Article
  14. Review
  15. 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

7 authors at 2 institutions in 1 country.

Yuanjie YuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-0924-0882
Tian TianDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Shiyun TanDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Pengbo WuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Yitian GuoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Ming LiDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-8601-9890
Mengjun HuangDepartment of Nutrition, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wuhan University · CNCentral Hospital of Wuhan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress and chronic inflammation are major culprits of nonalcoholic fatty liver disease (NAFLD). MicroRNA-665-3p (miR-665-3p) is implicated in regulating inflammation and oxidative stress; however, its role and molecular basis in NAFLD remain elusive. Herein, we measured a significant upregulation of miR-665-3p level in the liver and primary hepatocytes upon high fat diet (HFD) or 0.5 mmol/L palmitic acid plus 1.0 mmol/L oleic acid stimulation, and the elevated miR-665-3p expression aggravated oxidative stress, inflammation and NAFLD progression in mice. In contrast, miR-665-3p inhibition by the miR-665-3p antagomir significantly prevented HFD-induced oxidative stress, inflammation and hepatic dysfunction in vivo. Manipulation of miR-665-3p in primary hepatocytes also caused similar phenotypic alterations in vitro. Mechanistically, we demonstrated that miR-665-3p directly bound to the 3'-untranslated region of fibronectin type III domain-containing 5 (FNDC5) to downregulate its expression and inactivated the downstream AMP-activated protein kinase alpha (AMPKα) pathway, thereby facilitating oxidative stress, inflammation and NAFLD progression. Our findings identify miR-665-3p as an endogenous positive regulator of NAFLD via inactivating FNDC5/AMPKα pathway, and inhibiting miR-665-3p may provide novel therapeutic strategies to treat NAFLD.

Indexed as

Non-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesAnimalsAntagomirsCells, CulturedDisease ProgressionFibronectinsHEK293 CellsHepatocytesHumansLiverMaleMiceMice, Inbred C57BLMicroRNAsSignal TransductionAMP-Activated Protein KinasesAntagomirsFibronectinsFNDC5 protein, humanFNDC5 protein, mouseMicroRNAsMIRN665 microRNA, humanMIRN665 microRNA, mouseAMPKαFNDC5inflammationMir-665-3pNAFLDoxidative stress

Identifiers

PMID35038955
PMCPMC8973643
OpenAlexW4205485389

What Socratic 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 Socratic graph.