Evidence map›Paper›PMID 31157255›Full record

ArticleAnnals of translational medicine2019

Enhancing autophagy protects platelets in immune thrombocytopenia patients.

Chun-Yan Wang, Sai Ma, Shao-Jie Bi, Le Su, Shu-Ya Huang, Jun-Ying Miao, Chun-Hong Ma, Cheng-Jiang Gao, Ming Hou, Jun Peng

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Platelet Innate Immune Receptors and TLRs: A Double-Edged Sword.International journal of molecular sciences · 2021
    Review
  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

10 authors at 3 institutions in 1 country.

Chun-Yan WangDepartment of Geriatric Medicine, Second Hospital of Shandong University, Ji'nan 250033, China.
Sai MaDepartment of Hematology, Qilu Hospital, Shandong University, Ji'nan 250012, China.
Shao-Jie BiDepartment of Cardiology, Second Hospital of Shandong University, Ji'nan 250033, China.
Le SuShandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science, Shandong University, Ji'nan 250013, China.
Shu-Ya HuangShandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science, Shandong University, Ji'nan 250013, China.
Jun-Ying MiaoShandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science, Shandong University, Ji'nan 250013, China.
Chun-Hong MaDepartment of Immunology, Shandong University School of Medicine, Ji'nan 250012, China.
Cheng-Jiang GaoDepartment of Immunology, Shandong University School of Medicine, Ji'nan 250012, China.
Ming HouLeading Research Group of Scientific Innovation, Department of Science and Technology of Shandong Province, Ji'nan 250012, China.
Jun PengDepartment of Hematology, Qilu Hospital, Shandong University, Ji'nan 250012, China.
Shandong University · CNQilu Hospital of Shandong University · CNSecond Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune thrombocytopenia (ITP) is an autoimmune bleeding disorder and involves increased apoptosis of platelets. Autophagy is an essential process for platelets to maintain their life and physiological functions. However, the role of autophagy in ITP platelets was previously unclear.

methodsIn the present study, the expression of autophagy-related protein and autophagy flux were detected in platelets from ITP patients and healthy controls by immunofluorescence staining and immunoblotting, and the influence of autophagy on the viability and apoptosis of ITP platelets was further explored.

resultsWe found that platelet autophagy was diminished in ITP patients. Platelet autophagy in ITP was regulated by the PI3K/AKT/mTOR pathway, with mTOR (mammalian target of rapamycin) as a negative regulator and class III PtdIns3K playing a crucial role in the process. Importantly, the small-molecule compound ABO (6-amino-2,3-dihydro-3-hydroxymethyl-1,4-benzoxazine) enhanced autophagy in ITP platelets. Enhancing platelet autophagy alleviated platelet destruction by inhibiting apoptosis and improving platelet viability.

conclusionsThese results suggest a role for autophagy regulation in the pathogenesis of ITP, and offer a novel treatment for these patients.

Indexed as

6-amino-2,3-dihydro-3-hydroxymethyl-1,4-benzoxazine (ABO)autophagyImmune thrombocytopenia (ITP)

Identifiers

PMID31157255
PMCPMC6511561
OpenAlexW2939879841

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.