Evidence map›Paper›PMID 33968295›Full record

ArticleOxidative medicine and cellular longevity2021

Fisetin Alleviates Neointimal Hyperplasia via PPAR

Fang Pei, Hua Pei, Chunhua Su, Lin Du, Jifen Wang, Fusheng Xie, Qi Yin, Zhao Gao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Fisetin alleviates pulmonary arterial hypertension by inhibiting the TGF-β1/Smad 2/3 signaling pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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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

8 authors at 3 institutions in 1 country.

Fang PeiDepartment of Cardiology, Bishan District People's Hospital in Chongqing Municipality, Chongqing 402760, China.
Hua PeiClinical Lab, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570331, China.
Chunhua SuDepartment of Cardiology, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541199, China.
Lin DuMedical Laboratory, Xingyi People's Hospital, Xingyi, Guizhou 562400, China.
Jifen WangNeurology Department, Xingyi People's Hospital, Xingyi, Guizhou 562400, China.
Fusheng XieDepartment of Cardiology, The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541199, China.
Qi YinMedical and Healthcare Center, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, China.
Zhao GaoMedical and Healthcare Center, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570311, China.ORCID https://orcid.org/0000-0003-4870-0682
Guilin Medical University · CNHainan General Hospital · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenotypic transformation of proliferation and migration in vascular smooth muscle cells (VSMCs) from media to intima is the basic pathology of neointimal hyperplasia after angioplasty in hypertensive patients. Angiotensin II (AngII) stimulates oxidative stress in VSMC, inducing VSMC proliferation and migration, which is a critical factor in both developments of hypertension and angioplasty-induced arterial restenosis. Fisetin, a plant flavonoid polyphenol, has been reported to be antioxidative and potent senolytic. It is unknown whether fisetin would inhibit neointimal hyperplasia. Therefore, we investigated the role of fisetin in neointimal formation in vitro and in vivo. The rat thoracic aortic smooth muscle cells (A10 cells) stimulated by AngII were used as the in vitro neointimal hyperplasia model, where AngII significantly induced the proliferation and migration in A10 cells. We found that fisetin could dose-dependently inhibit the effect of AngII via inducing the expression of an antioxidant, paraoxonase-2 (PON2), whose overexpression could inhibit the proliferation and migration of A10 cells and downexpression by siRNA had the opposite effect. Furthermore, we found the mechanism of fisetin's inducing PON2 expression involved PPAR

Indexed as

AnimalsDisease Models, AnimalFlavonolsHyperplasiaPPAR gammaRatsfisetinFlavonolsPPAR gamma

Identifiers

PMID33968295
PMCPMC8084648
OpenAlexW3156643411

What OpenQuestion holds

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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.