Evidence map›Paper›PMID 40640354›Full record

ArticleCommunications biology2025

Fortilin deficiency induces anti-atherosclerotic phenotypes in macrophages and protects hypercholesterolemic mice against atherosclerosis.

Nattaporn Wanachottrakul, Decha Pinkaew, Sandipan Mukherjee, Preedakorn Chunhacha, Mari Nakashima, Asa A Brockman, Uttariya Pal, Hasseri B Halim, Yuhong Wei, Lena Tanaka and 5 more

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Nattaporn Wanachottrakul *Division of Cardiology, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Decha Pinkaew *Division of Cardiology, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Sandipan Mukherjee *Division of Cardiology, Department of Internal Medicine, University of Washington, Seattle, WA, USA.
Preedakorn Chunhacha *Division of Cardiology, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Mari NakashimaDivision of Cardiology, Department of Internal Medicine, University of Washington, Seattle, WA, USA.ORCID http://orcid.org/0009-0005-2237-645X
Asa A BrockmanDepartments of Cell & Developmental Biology and Neurological Surgery, Vanderbilt University School of Medicine, Nashville, TN, USA.ORCID http://orcid.org/0000-0002-0059-0392
Uttariya PalDivision of Cardiology, Department of Internal Medicine, University of Washington, Seattle, WA, USA.
Hasseri B HalimDivision of Cardiology, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA.ORCID http://orcid.org/0000-0002-2983-2607
Yuhong WeiRosalind and Morris Goodman Cancer Institute, McGill University, Montreal, Quebec, Canada.
Lena TanakaDivision of Cardiology, Department of Internal Medicine, University of Washington, Seattle, WA, USA.
Hanna HuynhDivision of Cardiology, Department of Internal Medicine, University of Washington, Seattle, WA, USA.ORCID http://orcid.org/0009-0007-0269-4631
Kota RamanaDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch at Galveston, Galveston, TX, USA.ORCID http://orcid.org/0000-0001-6502-7800
Shiyou ChenDepartment of Surgery, University of Missouri, Columbia, MO, USA.ORCID http://orcid.org/0000-0002-0297-8649
Rebecca A IhrieDepartments of Cell & Developmental Biology and Neurological Surgery, Vanderbilt University School of Medicine, Nashville, TN, USA.ORCID http://orcid.org/0000-0003-0439-0141
Ken FujiseDivision of Cardiology, Department of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA. kfujise@uw.edu.ORCID http://orcid.org/0000-0002-6763-8055

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Fortilin, p53, and atherosclerosisR01HL117247 · NHLBI · UNIVERSITY OF WASHINGTON · PI CHEN, SHIYOU, FUJISE, KEN · 2013 to 2023
$4.7M
Fortilin, CTNNA3, and the HeartR01HL152723 · NHLBI · UNIVERSITY OF WASHINGTON · PI FUJISE, KEN · 2021 to 2024
$2.7M
USING FORTILIN INHIBITORS TO BLOCK ATHEROSCLEROSISR01HL138992 · NHLBI · UNIVERSITY OF WASHINGTON · PI FUJISE, KEN, SRIVASTAVA, SANJAY · 2017 to 2020
$2.6M
Gut Dysbiosis and Cardiac Remodeling in IBDR01HL152683 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI FUJISE, KEN, LI, QINGJIE · 2020 to 2023
$2.6M
Identifying mTOR Dependent Periods During Brain DevelopmentR01NS118580 · NINDS · VANDERBILT UNIVERSITY · PI ESS, KEVIN C, IHRIE, REBECCA A · 2020 to 2024
$2.1M
RECK as a Therapeutic Target for AtherosclerosisR01HL170056 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI Chandrasekar Bysani, Shiyou Chen · 2025 to 2026
$1.3M
Characterization of Fortilin, A Novel Anti-p53 ProteinR01HL068024 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FUJISE, KEN · 2001 to 2005
$992k
American Heart Association (American Heart Association, Inc.) 25POST1374001NHLBI NIH HHS R01 HL068024NHLBI NIH HHS R01 HL117247NHLBI NIH HHS R01 HL138992NHLBI NIH HHS R01 HL152683NHLBI NIH HHS R01 HL152723NHLBI NIH HHS R01 HL170056NIDDK NIH HHS P30 DK017047NINDS NIH HHS R01 NS118580U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL117247U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL138992U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL152683U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL152723U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS118580
6 · The paper itself

Abstract

In the atherosclerotic intima, macrophages (MΦ) perpetuate chronic inflammation and cholesterol accumulation. Fortilin, a 172-amino-acid multifunctional protein, is abundant in the atherosclerotic intima and promotes atherogenesis, but its mechanism has remained unclear. Herein, we report that fortilin in MФ (fortilin

Indexed as

AtherosclerosisHypercholesterolemiaMacrophagesAnimalsCell ProliferationMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotype

Identifiers

PMID40640354
PMCPMC12246171

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.