Evidence mapPaperPMID 37115396Full record

ReviewCurrent medical science2023

From Diabetes to Diabetic Complications: Role of Autophagy.

Lin-Hua Wang, Yang-Yang Wang, Lian Liu, Quan Gong

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Article
  4. Targeting Autophagy: A Promising Therapeutic Strategy for Diabetes Mellitus and Diabetic Nephropathy.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024
    Review
  5. 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

4 authors at 1 institution in 1 country.

Lin-Hua Wang *Clinical Molecular Immunology Center, Yangtze University, Jingzhou, 434023, China.
Yang-Yang Wang *Clinical Molecular Immunology Center, Yangtze University, Jingzhou, 434023, China.
Lian LiuDepartment of Pharmacology, School of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, 434023, China. liulian@yangtzeu.edu.cn.
Quan GongClinical Molecular Immunology Center, Yangtze University, Jingzhou, 434023, China. gongquan1998@163.com.
Yangtze University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes and its complications reduce quality of life and are life-limiting. At present, diabetes treatment consists of hypoglycemic agents to control blood glucose and the use of insulin-sensitizing drugs to overcome insulin resistance. In diabetes, autophagy is impaired and thus there is poor intracellular environment homeostasis. Pancreatic β-cells and insulin target tissues are protected by enhancing autophagy. Autophagy decreases β-cell apoptosis, promotes β-cell proliferation, and alleviates insulin resistance. Autophagy in diabetes is regulated by the mammalian target of rapamycin (mTOR)/adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway and others. Autophagy enhancers can likely be used as a treatment for diabetes and its complications. This review examines the evidence linking autophagy to diabetes.

Indexed as

Diabetes MellitusInsulin ResistanceInsulinsAutophagyHumansQuality of LifeTOR Serine-Threonine KinasesInsulinsTOR Serine-Threonine Kinasesautophagydiabetesdiabetic complicationsmechanism

Identifiers

PMID37115396
OpenAlexW4367297567

What Socratic 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 Socratic graph.