Evidence map›Paper›PMID 33505579›Full record

ArticleOxidative medicine and cellular longevity2020

Fucoidan Inhibits NLRP3 Inflammasome Activation by Enhancing p62/SQSTM1-Dependent Selective Autophagy to Alleviate Atherosclerosis.

Yufei Cheng, Xudong Pan, Jing Wang, Xu Li, Shaonan Yang, Ruihua Yin, Aijun Ma, Xiaoyan Zhu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 61 citations in OpenAlex.

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  14. Investigating biochemical markers of Acupuncture's effectiveness in managing climacteric syndrome in breast cancer patients: the FLAIR study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
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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 1 institution in 1 country.

Yufei ChengDepartment of Neurology, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0001-9535-5602
Xudong PanDepartment of Neurology, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0002-4011-6812
Jing WangInstitute of Cerebrovascular Diseases, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0003-2184-3771
Xu LiInstitute of Cerebrovascular Diseases, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0003-4319-8953
Shaonan YangDepartment of Neurology, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0002-3426-3154
Ruihua YinDepartment of Neurology, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0002-8691-9530
Aijun MaDepartment of Neurology, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0001-6359-8562
Xiaoyan ZhuDepartment of Critical Care Medicine, The Affiliated Hospital of Qingdao University, Shandong 266100, China.ORCID https://orcid.org/0000-0001-9616-9289
Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation contributes to the progression of atherosclerosis, and autophagy inhibits inflammasome activation by targeting macrophages. We investigated whether fucoidan, a marine sulfated polysaccharide derived from brown seaweeds, could reduce NLRP3 inflammasome activation by enhancing sequestosome 1 (p62/SQSTM1)-dependent selective autophagy to alleviate atherosclerosis in high-fat-fed ApoE-/- mice with partial carotid ligation and differentiated THP-1 cells incubated with oxidized low-density lipoprotein (oxLDL). Fucoidan significantly ameliorated lipid accumulation, attenuated progression of carotid atherosclerotic plaques, deregulated the expression of NLRP3 inflammasome, autophagy receptor p62, and upregulated microtubule-associated protein light chain 3 (LC3)-II/I levels. Transmission electron microscopy and GFP-RFP-LC3 lentivirus transfection further demonstrated that fucoidan could activate autophagy. Mechanistically, fucoidan remarkably inhibited NLRP3 inflammasome activation, which was mostly dependent on autophagy. The inhibitory effects of fucoidan on NLRP3 inflammasome were enhanced by autophagy activator rapamycin (Rapa) and alleviated by autophagy inhibitor 3-methyladenine (3-MA). Fucoidan promoted the colocalization of NLRP3 and p62. Knockdown of p62 and ATG5 by small interfering RNA significantly reduced the inhibitory effects of fucoidan treatment on NLRP3 inflammasome. The data suggest that fucoidan can inhibit NLRP3 inflammasome activation by enhancing p62/SQSTM1-dependent selective autophagy to alleviate atherosclerosis.

Indexed as

AdenineAnimalsAtherosclerosisAutophagosomesAutophagyAutophagy-Related Protein 5Gene Knockdown TechniquesHumansInflammasomesLipid MetabolismLipoproteins, LDLMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout3-methyladenineAdenineAutophagy-Related Protein 5fucoidanInflammasomesLipoproteins, LDLMAP1LC3A protein, humanMap1lc3b protein, mouseMicrotubule-Associated ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNlrp3 protein, mouseoxidized low density lipoproteinPolysaccharidesSequestosome-1 ProteinSirolimusSQSTM1 protein, humanSqstm1 protein, mouse

Identifiers

PMID33505579
PMCPMC7812546
OpenAlexW3047084319

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.