Evidence map›Paper›PMID 37065747›Full record

ReviewFrontiers in endocrinology2023

The relationship between HMGB1 and autophagy in the pathogenesis of diabetes and its complications.

Kun Yang, Feng Cao, Weili Wang, Zhenyu Tian, Lu Yang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.7field-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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Role of HMGB1 on the onset of preeclampsia.BMC pregnancy and childbirth · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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
  13. Article
  14. Article
  15. Article
  16. Frontiers in pharmacology · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Kun YangCollege of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Feng CaoCollege of Acupuncture and Massage, Beijing University of Chinese Medicine, Beijing, China.
Weili WangInstitute of Basic Research in Clinical Traditional Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing, China.
Zhenyu TianThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Lu YangCollege of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNTianjin University of Traditional Chinese Medicine · CNCommunity Health Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose levels and has become the third leading threat to human health after cancer and cardiovascular disease. Recent studies have shown that autophagy is closely associated with diabetes. Under normal physiological conditions, autophagy promotes cellular homeostasis, reduces damage to healthy tissues and has bidirectional effects on regulating diabetes. However, under pathological conditions, unregulated autophagy activation leads to cell death and may contribute to the progression of diabetes. Therefore, restoring normal autophagy may be a key strategy to treat diabetes. High-mobility group box 1 protein (HMGB1) is a chromatin protein that is mainly present in the nucleus and can be actively secreted or passively released from necrotic, apoptotic, and inflammatory cells. HMGB1 can induce autophagy by activating various pathways. Studies have shown that HMGB1 plays an important role in insulin resistance and diabetes. In this review, we will introduce the biological and structural characteristics of HMGB1 and summarize the existing knowledge on the relationship between HMGB1, autophagy, diabetes, and diabetic complications. We will also summarize potential therapeutic strategies that may be useful for the prevention and treatment of diabetes and its complications.

Indexed as

Diabetes ComplicationsDiabetes MellitusHMGB1 ProteinInsulin ResistanceAutophagyCell DeathHumansHMGB1 ProteinHMGB1 protein, humanautophagydiabetesdiabetic complicationHMGB1TCM

Identifiers

PMID37065747
PMCPMC10090453
OpenAlexW4361201344

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.