Evidence map›Paper›PMID 40047069›Full record

ArticleCirculation research2025

LncRNA MIR181A1HG Deficiency Attenuates Vascular Inflammation and Atherosclerosis.

Huaner Ni, Yulong Ge, Ying Zhuge, Xiaoqiang Liu, Hangwei Chen, Junyi Liu, Weifeng Li, Xiang Wang, Gu Shen, Qiuling Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025
    Review
  17. TheNon-coding RNA · 2025
    Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Huaner Ni *Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0002-9651-3411
Yulong Ge *Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0002-3541-7354
Ying Zhuge *Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0003-2952-4302
Xiaoqiang Liu *Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0003-0108-5918
Hangwei ChenDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0002-1057-3772
Junyi LiuDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0001-5667-7983
Weifeng LiDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).
Xiang WangDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).
Gu ShenDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).
Qiuling WangDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).
Rulin ZhuangDepartment of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, China (R.Z.).
Mark W FeinbergDepartment of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (M.W.F.).ORCID 0000-0001-9523-3859
Fang WangDepartment of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).ORCID 0000-0001-8367-8973

Funding

MiR-181b, endothelial cells, and vascular inflammationR01HL115141 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2012 to 2024
$6.8M
NHLBI NIH HHS R01 HL115141
6 · The paper itself

Abstract

backgroundEndothelial cell (EC) dysfunction and vascular inflammation are critical in the initiation and progression of atherosclerosis. Long noncoding RNAs play a critical role in vascular pathology, but relatively little is known about their involvement in controlling vascular inflammation. MIR181A1HG is a conserved long noncoding RNA located in juxtaposition with miR-181a1 and miR-181b1, both involved in vascular inflammation. The study aims to investigate the role of MIR181A1HG in regulating vascular inflammation.

methodsWe examined the expression of MIR181A1HG in both human and mouse atherosclerotic lesions. Loss-of-function and gain-of-function studies, and multiple RNA-protein interaction assays were used to investigate the role and molecular mechanisms of MIR181A1HG in vascular inflammation and atherosclerosis. The atherosclerotic phenotypes of MIR181A1HG

resultsMIR181A1HG expression was abundant in ECs and significantly increased in both human and mouse atherosclerotic lesions. MIR181A1HG

conclusionsThese findings identify MIR181A1HG as a central driver of vascular inflammation in atherosclerosis by its ability to decoy Foxp1 away from target gene promoters and activate NLRP3 inflammasome in the vascular endothelium. Our study suggests MIR181A1HG as a future therapeutic target for vascular inflammatory disease states.

Indexed as

AtherosclerosisMicroRNAsRNA, Long NoncodingVasculitisAnimalsCells, CulturedEndothelial CellsHumansInflammasomesMaleMiceMice, Inbred C57BLMice, Knockout, ApoENLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionTranscription Factor RelAInflammasomesMicroRNAsmirn181 microRNA, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseRNA, Long NoncodingTranscription Factor RelAatherosclerosiscardiovascular diseasesendothelial cellsinflammasomesRNA, long noncoding

Identifiers

PMID40047069
PMCPMC11985291

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.