Evidence map›Paper›PMID 40707465›Full record

ArticleCell death & disease2025

The accumulation of progerin underlies the loss of aortic smooth muscle cells in Hutchinson-Gilford progeria syndrome.

Paul H Kim, Joonyoung R Kim, Patrick J Heizer, Hyesoo Jung, Yiping Tu, Ashley Presnell, Julia Scheithauer, Rachel G Yu, Stephen G Young, Loren G Fong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Prelamin A in anArteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Precise progerin targeting using RfxCas13d: A therapeutic avenue for Hutchinson-Gilford progeria syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Paul H KimDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-8429-651X
Joonyoung R KimDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Patrick J HeizerDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Hyesoo JungDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Yiping TuDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Ashley PresnellDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Julia ScheithauerDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Rachel G YuDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Stephen G YoungDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. sgyoung@mednet.ucla.edu.ORCID http://orcid.org/0000-0001-7270-3176
Loren G FongDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, USA. lfong@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-4465-5290

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
Investigating Mechanisms for Lipid Transport in Health and DiseaseR35HL139725 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2018 to 2024
$6.1M
Regulation of Intravascular Triglyceride HydrolysisR35HL176438 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Stephen G. Young · 2025 to 2026
$2.2M
Solving longstanding mysteries in plasma triglyceride metabolismR01HL171737 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANNE BEIGNEUX, Loren Gi Fong · 2024 to 2026
$1.9M
NHLBI NIH HHS R01 HL171737NHLBI NIH HHS R35 HL139725NHLBI NIH HHS R35 HL176438NIDDK NIH HHS P30 DK041301U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL139725U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL171737
6 · The paper itself

Abstract

Hutchinson-Gilford progeria syndrome (HGPS) is caused by progerin, an internally truncated prelamin A that does not undergo the ZMPSTE24 processing step that releases prelamin A's farnesylated carboxyl terminus; consequently, progerin remains farnesylated. Progerin and full-length farnesyl-prelamin A are equivalent in their abilities to disrupt the nuclear lamina and trigger nuclear membrane ruptures and cell death, but they differ markedly in their abilities to cause arterial pathology. In HGPS mice (Lmna

Indexed as

AortaLamin Type AMyocytes, Smooth MuscleProgeriaProtein PrecursorsAnimalsHumansMembrane ProteinsMetalloendopeptidasesMiceMice, KnockoutMuscle, Smooth, VascularProto-Oncogene Proteins c-aktLamin Type AMembrane ProteinsMetalloendopeptidasesprelamin AProtein PrecursorsProto-Oncogene Proteins c-aktZmpste24 protein, mouse

Identifiers

PMID40707465
PMCPMC12290114

What OpenQuestion holds

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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.