Evidence map›Paper›PMID 36028501›Full record

ArticleCell death & disease2022

SerpinE1 drives a cell-autonomous pathogenic signaling in Hutchinson-Gilford progeria syndrome.

Giorgia Catarinella, Chiara Nicoletti, Andrea Bracaglia, Paola Procopio, Illari Salvatori, Marilena Taggi, Cristiana Valle, Alberto Ferri, Rita Canipari, Pier Lorenzo Puri and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
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  3. SERPINE1 in ARDS: an emerging regulator of inflammation-coagulation-fibrinolysis crosstalk.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

11 authors at 6 institutions in 3 countries.

Giorgia CatarinellaIRCCS Fondazione Santa Lucia, Rome, Italy.
Chiara Nicoletti *Development, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, 92037, USA.
Andrea Bracaglia *IRCCS Fondazione Santa Lucia, Rome, Italy.
Paola ProcopioIRCCS Fondazione Santa Lucia, Rome, Italy.
Illari SalvatoriIRCCS Fondazione Santa Lucia, Rome, Italy.
Marilena TaggiDAHFMO, Unit of Histology and Medical Embryology, Sapienza, University of Rome, Rome, Italy.
Cristiana ValleIRCCS Fondazione Santa Lucia, Rome, Italy.
Alberto FerriIRCCS Fondazione Santa Lucia, Rome, Italy.
Rita CanipariDAHFMO, Unit of Histology and Medical Embryology, Sapienza, University of Rome, Rome, Italy.
Pier Lorenzo PuriDevelopment, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, 92037, USA.
Lucia LatellaIRCCS Fondazione Santa Lucia, Rome, Italy. lucia.latella@ift.cnr.it.ORCID 0000-0003-1317-9233
Istituto di Farmacologia Traslazionale · ITFondazione Santa Lucia · ITSanford Burnham Prebys Medical Discovery Institute · USSapienza University of Rome · ITPhilipps University of Marburg · DEUniversity of Rome Tor Vergata · IT

Funding

Role of STAT3 in muscle stem cell activationR01AR064873 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SACCO, ALESSANDRA · 2014 to 2018
$2.1M
NIAMS NIH HHS R01 AR064873
6 · The paper itself

Abstract

Hutchinson-Gilford progeria syndrome (HGPS) is a rare, fatal disease caused by Lamin A mutation, leading to altered nuclear architecture, loss of peripheral heterochromatin and deregulated gene expression. HGPS patients eventually die by coronary artery disease and cardiovascular alterations. Yet, how deregulated transcriptional networks at the cellular level impact on the systemic disease phenotype is currently unclear. A genome-wide analysis of gene expression in cultures of primary HGPS fibroblasts identified SerpinE1, also known as Plasminogen Activator Inhibitor (PAI-1), as central gene that propels a cell-autonomous pathogenic signaling from the altered nuclear lamina. Indeed, siRNA-mediated downregulation and pharmacological inhibition of SerpinE1 by TM5441 could revert key pathological features of HGPS in patient-derived fibroblasts, including re-activation of cell cycle progression, reduced DNA damage signaling, decreased expression of pro-fibrotic genes and recovery of mitochondrial defects. These effects were accompanied by the correction of nuclear abnormalities. These data point to SerpinE1 as a novel potential effector and target for therapeutic interventions in HGPS pathogenesis.

Indexed as

Plasminogen Activator Inhibitor 1ProgeriaCell NucleusFibroblastsHumansLamin Type ALamin Type APlasminogen Activator Inhibitor 1SERPINE1 protein, human

Identifiers

PMID36028501
PMCPMC9418244
OpenAlexW4293116325

What OpenQuestion holds

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LicenceCC BY
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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.