Evidence map›Paper›PMID 35903524›Full record

ArticleSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2022

Genistein promotes M1 macrophage apoptosis and reduces inflammatory response by disrupting miR-21/TIPE2 pathway.

Li Cong, Xiaolin Xie, Sujuan Liu, Liping Xiang, Xiaohua Fu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. TIPE2: a novel regulatory factor for cardiovascular-related diseases.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

5 authors at 1 institution in 1 country.

Li CongKey Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Changsha 410013, China.
Xiaolin XieSchool of Medicine, Hunan Normal University, Changsha 410013, China.
Sujuan LiuSchool of Medicine, Hunan Normal University, Changsha 410013, China.
Liping XiangSchool of Medicine, Hunan Normal University, Changsha 410013, China.
Xiaohua FuSchool of Medicine, Hunan Normal University, Changsha 410013, China.
Hunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases are a major cause of mortality, and vascular injury, a common pathological basis of cardiovascular disease, is deeply correlated with macrophage apoptosis and inflammatory response. Genistein, a type of phytoestrogen, exerts cardiovascular protective activities, but the underlying mechanism has not been fully elucidated. In this study, RAW264.7 cells were treated with genistein, lipopolysaccharide (LPS), nuclear factor-kappa B (NF-κB) inhibitor, and/or protein kinase B (AKT) agonist to determine the role of genistein in apoptosis and inflammation in LPS-stimulated cells. Simultaneously, high fat diet-fed C57BL/6 mice were administered genistein to evaluate the function of genistein on LPS-induced cardiovascular injury mouse model. Here, we demonstrated that LPS obviously increased apoptosis resistance and inflammatory response of macrophages by promoting miR-21 expression, and miR-21 downregulated tumor necrosis factor-α-induced protein 8-like 2 (TIPE2) expression by targeting the coding region. Genistein reduced miR-21 expression by inhibiting NF-κB, then blocked toll-like receptor 4 (TLR4) pathway and AKT phosphorylation dependent on TIPE2, resulting in inhibition of LPS. Our research suggests that miR-21/TIPE2 pathway is involved in M1 macrophage apoptosis and inflammatory response, and genistein inhibits the progression of LPS-induced cardiovascular injury at the epigenetic level via regulating the promoter region of Vmp1 by NF-κB.

Indexed as

3′ UTR, 3′ untranslated regionABCG1, ATP‐binding cassette transporter G1AKT, protein kinase BAP-1, activating protein-1BAX, BCL-2 associated XBCL-2, B cell lymphoma-2CCK-8, cell counting kit-8ChIP, chromatin immunoprecipitationCHOP, C/EBP homologous proteinCOX-2, cyclooxygenase-2CVDs, cardiovascular diseasesDMEM, Dulbecco's modified eagle's mediumELISA, enzyme-linked immunosorbent assayFBS, fetal bovine serumGEN, genisteinGenisteinHSP90, heat shock protein 90IF, immunofluorescenceIGF-1, insulin-like growth factor-1IL-6, interleukin 6Inflammatory responseiNOS, inducible nitric oxide synthaseJNK, c-Jun N-terminal kinaseLDH, lactate dehydrogenaseLipopolysaccharideLPS, lipopolysaccharideMacrophage apoptosismiR-21MUT, mutantMyD88, myeloid differentiation primary response 88NF-κB, nuclear factor-kappa BPBMCs, peripheral blood mononuclear cellsPBS, phosphate buffered salinePDCD4, programmed cell death 4PDTC, pyrrolidine dithiocarbamatePMφs, peritoneal macrophagesqRT-PCR, quantitative real-time polymerase chain reactionSTAT3, signal transducer and activator of transcription 3TiO2 NPs, titanium dioxide nanoparticlesTIPE2, tumor necrosis factor-α-induced protein 8-like 2TLR4, toll-like receptor 4TNF-α, tumor necrosis factor-αTRIF, Toll/IL-1R domain-containing adaptor-inducing IFN-βTumor necrosis factor-α-induced protein 8-like 2WT, wild type

Identifiers

PMID35903524
PMCPMC9315303
OpenAlexW4281384197

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.