Evidence map›Paper›PMID 34490483›Full record

ArticleMolecular medicine reports2021

Salvianolic acid B improves autophagic dysfunction and decreases the apoptosis of cholesterol crystal‑induced macrophages via inhibiting the Akt/mTOR signaling pathway.

Mengqi Sun, Yun Ye, Yilan Huang, Wenxian Yin, Zhaolan Yu, Shurong Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. 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

6 authors at 2 institutions in 1 country.

Mengqi Sun *Drug Clinical Trial Institution, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yun Ye *Department of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yilan HuangDepartment of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Wenxian YinDepartment of Pharmacy, The Affiliated Hospital of Traditional Chinese Medicine Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Zhaolan YuDepartment of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Shurong WangDepartment of Pharmacy, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Affiliated Hospital of Southwest Medical University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive macrophage dysfunction and apoptosis are some of the major events that occur during atherogenesis. To further investigate the intrinsic association between atherosclerosis (AS) and macrophage apoptosis and autophagy, cholesterol crystals (CHCs) were used to stimulate RAW264.7 macrophages to establish a macrophage model of advanced AS. Cells in the CHC group were treated with salvianolic acid B (Sal B) to evaluate its protective effects and reveal its underlying molecular mechanism. The results demonstrated that treatments with Sal B significantly improved autophagy dysfunction and reduced the apoptotic rate of CHC‑induced macrophages. Furthermore, Sal B significantly attenuated CHC‑induced release of proinflammatory factors (TNF‑α and IL‑6) by macrophages. Treatment of macrophages with a specific inhibitor of autophagy (3‑methyladenine) significantly reversed Sal B‑mediated effects on autophagy, suggesting that Sal B‑induced autophagy may display a protective effect in CHC‑induced macrophages. Furthermore, pretreatment of CHC‑induced macrophages with insulin significantly decreased Sal B‑induced autophagy, indicating that the Akt/mTOR signaling pathway may serve as a critical mediator in regulating Sal B‑mediated cell death. Taken together, the present study demonstrated that Sal B improved autophagic dysfunction and reduced the apoptosis of CHC‑induced macrophages via inhibiting the Akt/mTOR signaling pathway.

Indexed as

AnimalsApoptosisAtherosclerosisAutophagyBenzofuransDepsidesDrugs, Chinese HerbalMacrophagesMiceProtective AgentsProto-Oncogene Proteins c-aktRAW 264.7 CellsSalvia miltiorrhizaTOR Serine-Threonine KinasesBenzofuransDepsidesDrugs, Chinese HerbalMTOR protein, humanProtective AgentsProto-Oncogene Proteins c-aktsalvianolic acid BTOR Serine-Threonine KinasesapoptosisatherosclerosisautophagyRAW264.7 macrophagessalvianolic acid B

Identifiers

PMID34490483
PMCPMC8430306
OpenAlexW3198887301

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.