Evidence map›Paper›PMID 28191279›Full record

ArticleOxidative medicine and cellular longevity2017

ROS-Dependent Activation of Autophagy through the PI3K/Akt/mTOR Pathway Is Induced by Hydroxysafflor Yellow A-Sonodynamic Therapy in THP-1 Macrophages.

Yueqing Jiang, Jiayuan Kou, Xiaobo Han, Xuesong Li, Zhaoyu Zhong, Zhongni Liu, Yinghong Zheng, Ye Tian, Liming Yang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Sonodynamic therapy for the treatment of atherosclerosis.Journal of pharmaceutical analysis · 2024
    Review
  9. Nanomedicine for Diagnosis and Treatment of Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  10. The role of cell death in SARS-CoV-2 infection.Signal transduction and targeted therapy · 2023
    Review
  11. Sonocatalytic Optimization of Titanium-Based Therapeutic Nanomedicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  12. Recent Advances for Dynamic-Based Therapy of Atherosclerosis.International journal of nanomedicine · 2023
    Review
  13. Review
  14. Tuning macrophages for atherosclerosis treatment.Regenerative biomaterials · 2023
    Review
  15. Emerging Sonodynamic Therapy-Based Nanomedicines for Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

9 authors at 1 institution in 1 country.

Yueqing JiangDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Jiayuan KouDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Xiaobo HanDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Xuesong LiDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Zhaoyu ZhongDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Zhongni LiuDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Yinghong ZhengDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.
Ye TianDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China; Division of Cardiology, The First Affiliated Hospital, Harbin Medical University, Harbin, China.
Liming YangDepartment of Pathophysiology, Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin, China.ORCID 0000-0002-0390-8845
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocyte-derived macrophages participate in infaust inflammatory responses by secreting various types of proinflammatory factors, resulting in further inflammatory reactions in atherosclerotic plaques. Autophagy plays an important role in inhibiting inflammation; thus, increasing autophagy may be a therapeutic strategy for atherosclerosis. In the present study, hydroxysafflor yellow A-mediated sonodynamic therapy was used to induce autophagy and inhibit inflammation in THP-1 macrophages. Following hydroxysafflor yellow A-mediated sonodynamic therapy, autophagy was induced as shown by the conversion of LC3-II/LC3-I, increased expression of beclin 1, degradation of p62, and the formation of autophagic vacuoles. In addition, inflammatory factors were inhibited. These effects were blocked by Atg5 siRNA, the autophagy inhibitor 3-methyladenine, and the reactive oxygen species scavenger N-acetyl cysteine. Moreover, AKT phosphorylation at Ser473 and mTOR phosphorylation at Ser2448 decreased significantly after HSYA-SDT. These effects were inhibited by the PI3K inhibitor LY294002, the AKT inhibitor triciribine, the mTOR inhibitor rapamycin, mTOR siRNA, and N-acetyl cysteine. Our results demonstrate that HSYA-SDT induces an autophagic response via the PI3K/Akt/mTOR signaling pathway and inhibits inflammation by reactive oxygen species in THP-1 macrophages.

Indexed as

AutophagyBlotting, WesternCell LineCell SurvivalChalconeEnzyme-Linked Immunosorbent AssayFluorescent Antibody TechniqueGene Knockdown TechniquesHumansMacrophagesMicroscopy, Electron, TransmissionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinonesReactive Oxygen SpeciesSignal TransductionChalconehydroxysafflor yellow AMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinonesReactive Oxygen SpeciesTOR Serine-Threonine Kinases

Identifiers

PMID28191279
PMCPMC5278230
OpenAlexW2578205996

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.