Evidence map›Paper›PMID 40747550›Full record

ArticleHypertension (Dallas, Tex. : 1979)2025

Cellular Senescence Mediates Doxorubicin Chemotherapy-Induced Aortic Stiffening: Role of Glycation Stress.

Ravinandan Venkatasubramanian, Mary A Darrah, Sophia A Mahoney, David A Hutton, Grace S Maurer, Katelyn R Ludwig, Nicholas S Van Dongen, Nathan T Greenberg, Abigail G Longtine, Vienna E Brunt and 8 more

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Article in Hypertension (Dallas, Tex. : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Ravinandan VenkatasubramanianDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).
Mary A DarrahDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0009-0003-8358-7205
Sophia A MahoneyDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0002-0013-4514
David A HuttonDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0002-5827-6953
Grace S MaurerDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0002-6952-5097
Katelyn R LudwigDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).
Nicholas S Van DongenDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).
Nathan T GreenbergDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0001-5174-3195
Abigail G LongtineDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0001-7905-8341
Vienna E BruntDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0002-1941-7936
Parminder SinghBuck Institute for Research on Aging, Novato, CA (P.S., P.K., S.M.).
James J GalliganDepartment of Pharmacology and Toxicology, University of Arizona, Tucson (J.J.G., M.N.T.).ORCID 0000-0002-5612-0680
Marissa N TrujilloDepartment of Pharmacology and Toxicology, University of Arizona, Tucson (J.J.G., M.N.T.).
Pankaj KapahiBuck Institute for Research on Aging, Novato, CA (P.S., P.K., S.M.).ORCID 0000-0002-5629-4947
Simon MelovBuck Institute for Research on Aging, Novato, CA (P.S., P.K., S.M.).ORCID 0000-0001-8554-2834
Matthew J RossmanDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0001-9381-2590
Douglas R SealsDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0002-2391-9824
Zachary S ClaytonDepartment of Integrative Physiology, University of Colorado Boulder (R.V., M.A.D., S.A.M., D.A.H., G.S.M., K.R.L., N.S.V.D., N.T.G., A.G.L., V.E.B., M.J.R., D.R.S., Z.S.C.).ORCID 0000-0003-3878-3533

Funding

Role of cellular senescence in cardiovascular agingR01AG055822 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH, MELOV, SIMON · 2018 to 2022
$4.9M
Establishing Glyoxalase 2 as a Viable Target for the Treatment of Disease [Equipment Supplement]R35GM137910 · NIGMS · UNIVERSITY OF ARIZONA · PI GALLIGAN, JAMES J · 2020 to 2024
$2.1M
Glyoxalase 1 and its Role in Metabolic SyndromeR01DK133196 · NIDDK · UNIVERSITY OF ARIZONA · PI James J Galligan · 2023 to 2026
$1.8M
Targeting cellular senescence to prevent accelerated vascular aging induced by the common chemotherapeutic agent doxorubicinR21AG078408 · NIA · UNIVERSITY OF COLORADO · PI SEALS, DOUGLAS R · 2022 to 2023
$430k
Translational studies of cellular senescence as a regulator of doxorubicin-mediated arterial dysfunctionK99HL159241 · NHLBI · UNIVERSITY OF COLORADO · PI CLAYTON, ZACHARY S. · 2022 to 2023
$350k
NHLBI NIH HHS K99 HL159241NIA NIH HHS R01 AG055822NIA NIH HHS R21 AG078408NIDDK NIH HHS R01 DK133196NIGMS NIH HHS R35 GM137910
6 · The paper itself

Abstract

backgroundMechanisms underlying doxorubicin chemotherapy-induced aortic stiffening are incompletely understood. To determine the role of cellular senescence and the senescence-associated secretory phenotype (SASP) in mediating doxorubicin-induced aortic stiffening and the influence of senolytic therapy.

methodsAortic stiffness (aortic pulse wave velocity) and associated mechanisms were assessed in young adult p16-3MR mice, a model that allows for genetic-based clearance of senescent cells with ganciclovir. Young (4-6 months) mice were injected with doxorubicin and subsequently treated with ganciclovir or the senolytic ABT263. We evaluated the influence of SASP-associated circulating factors in plasma (the circulating SASP milieu) in mediating aortic stiffening ex vivo (aortic elastic modulus) and examined the contribution of glycation stress.

resultsDoxorubicin increased aortic pulse wave velocity (425±6 versus control, 353±5 cm/s;

conclusionsCellular senescence and the circulating SASP milieu contribute to doxorubicin-induced aortic stiffening. Senolytics hold promise for preserving aortic stiffening following doxorubicin exposure.

Indexed as

Antibiotics, AntineoplasticAortaCellular SenescenceDoxorubicinSenescence-Associated Secretory PhenotypeVascular StiffnessAniline CompoundsAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLPulse Wave AnalysisSenotherapeuticsSulfonamidesAniline CompoundsAntibiotics, AntineoplasticDoxorubicinnavitoclaxSenotherapeuticsSulfonamidesanimalselastic modulusnavitoclaxpulse wave analysisvascular stiffness

Identifiers

PMID40747550
PMCPMC12327803

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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.