Evidence map›Paper›PMID 27825897›Full record

ReviewAgeing research reviews2017

The senescence accelerated mouse prone 8 (SAMP8): A novel murine model for cardiac aging.

Vengadeshprabhu Karuppagounder, Somasundaram Arumugam, Sahana Suresh Babu, Suresh S Palaniyandi, Kenichi Watanabe, John P Cooke, Rajarajan A Thandavarayan

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  6. ATF3 Deficiency Exacerbates Ageing-Induced Atherosclerosis and Clinical Intervention Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  9. Review
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  17. The immunology of heart failure with preserved ejection fraction.Clinical science (London, England : 1979) · 2023
    Review
  18. Article
  19. Review
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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

7 authors at 3 institutions in 2 countries.

Vengadeshprabhu KaruppagounderDepartment of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Somasundaram ArumugamDepartment of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Sahana Suresh BabuDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, USA.
Suresh S PalaniyandiDivision of Hypertension and Vascular Research, Henry Ford Health System, Detroit, MI 48202, USA.
Kenichi WatanabeDepartment of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
John P CookeDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, USA.
Rajarajan A ThandavarayanDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, USA. Electronic address: ramirthalingamthandavarayan@houstonmethodist.org.
Houston Methodist · USNiigata University of Pharmacy and Applied Life Sciences · JPHenry Ford Health System · US

Funding

Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
American Heart Association-American Stroke Association 15POST25710392NHLBI NIH HHS U01 HL100397
6 · The paper itself

Abstract

Because cardiovascular disease remains the major cause of mortality and morbidity world-wide, there remains a compelling need for new insights and novel therapeutic avenues. In this regard, the senescence-accelerated mouse prone 8 (SAMP8) line is a particularly good model for studying the effects of aging on cardiovascular health. Accumulating evidence suggests that this model may shed light on age-associated cardiac and vascular dysfunction and disease. These animals manifest evidence of inflammation, oxidative stress and adverse cardiac remodeling that may recapitulate processes involved in human disease. Early alterations in oxidative damage promote endoplasmic reticulum stress to trigger apoptosis and cytokine production in this genetically susceptible mouse strain. Conversely, pharmacological treatments that reduce inflammation and oxidative stress improve cardiac function in these animals. Therefore, the SAMP8 mouse model provides an exciting opportunity to expand our knowledge of aging in cardiovascular disease and the potential identification of novel targets of treatment. Herein, we review the previous studies performed in SAMP8 mice that provide insight into age-related cardiovascular alterations.

Indexed as

Aging, PrematureCardiovascular SystemAnimalsApoptosisCellular SenescenceDisease Models, AnimalInflammationMiceOxidative StressAgingCardiac remodelingInflammationOxidative stressSenescence-accelerated prone mouse 8

Identifiers

PMID27825897
PMCPMC12142494
OpenAlexW2548968391

What OpenQuestion 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 OpenQuestion graph.