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Peer-reviewedCC BY 4.0Frontiers in Cardiovascular Medicine

Age-related cardiac dysfunction is not associated with shorter telomere length in laboratory rats

  • Sindre T. Strandberg1,2
  • Trine B. Opstad1,2
  • Andreas Romaine2,3
  • Emil Espe4
  • Mani Sadredini4,5
  • Kari Gulbrandsen Løken4
  • Sheryl Palmero1
  • Jørgen A. Gravning1,2
  • Ivar Sjaastad4
  • Ida G. Lunde1,2,6
  • Mathis K. Stokke4
  • Ragnhild Helseth1
6 affiliations
  1. 1Oslo Center for Clinical Heart Research (Oslo-CCHR), Department of Cardiology Ullevaal, Oslo University Hospital
  2. 2University of Oslo
  3. 3Institute for Surgical Research, Oslo University Hospital
  4. 4Institute for Experimental Medical Research (IEMR), University of Oslo and Oslo University Hospital
  5. 5Department of Nursing and Health Promotion, Faculty of Health Sciences, Oslo Metropolitan University
  6. 6KG Jebsen Center for Cardiac Biomarkers, Institute of Clinical Medicine, University of Oslo
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Abstract

Introduction: Ageing is an independent risk factor for cardiovascular disease (CVD). Preclinical models of ageing are needed to better understand human diseases. Telomere shortening is a critical process in cellular ageing and senescence. In humans, it is well-established that telomere shortening in circulating leukocytes is associated with CVD, however, whether this applies to common preclinical models remains disputable. We investigated leukocyte telomere length (LTL), cardiac telomere length (CTL), and age-related cardiac remodeling and functional decline in commonly used laboratory rats.

Methods: Sprague-Dawley rats ( n = 51) were euthanized at 3, 9, 16, or 24 months (mo), respectively. Cardiac function was assessed by echocardiography. Relative telomere length, mRNA levels of telomerase and signature genes involved in inflammation and fibrosis were quantified in circulating leukocytes and left ventricular tissue by quantitative or digital droplet PCR (qPCR or ddPCR, respectively).

Results: Rats with increasing chronological age (16/24 months compared to 9 months) exhibited cardiac hypertrophy and diastolic dysfunction, as evidenced by increased septal and posterior wall thickness, and elevated E/e’ ratio, and increased cardiac expression of central inflammatory ( Il6 ) and fibrotic ( Ctgf ) genes. Relative LTL and CTL remained unchanged across chronological age groups (LTL: 9 months 1.000 vs. 16 months 0.939 vs. 24 months 1.120, p = 0.37; and CTL: 9 months 1.000 vs. 16 months 1.021 vs. 24 months 0.897, p = 0.42). CTL and LTL did not correlate ( r = −0.027, p = 0.89). No association with cardiac dysfunction was observed, neither for LTL nor CTL.

Discussion: Laboratory rats of high age exhibited cardiac hypertrophy and dysfunction, resembling human cardiac ageing, however we found no evidence of shorter telomere lengths in circulating leukocytes nor cardiac cells, suggesting a translational gap.

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Cite

BibTeXRIS
BibTeX
@article{strandberg2026agerelated,
  title = {{Age-related cardiac dysfunction is not associated with shorter telomere length in laboratory rats}},
  author = {Sindre T. Strandberg and Trine B. Opstad and Andreas Romaine and Emil Espe and Mani Sadredini and Kari Gulbrandsen Løken and Sheryl Palmero and Jørgen A. Gravning and Ivar Sjaastad and Ida G. Lunde and Mathis K. Stokke and Ragnhild Helseth},
  journal = {Frontiers in Cardiovascular Medicine},
  year = {2026},
  month = oct,
  doi = {10.3389/fcvm.2026.1790767},
  url = {https://www.frontiersin.org/articles/10.3389/fcvm.2026.1790767/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Age-related cardiac dysfunction is not associated with shorter telomere length in laboratory rats
AU  - Sindre T. Strandberg
AU  - Trine B. Opstad
AU  - Andreas Romaine
AU  - Emil Espe
AU  - Mani Sadredini
AU  - Kari Gulbrandsen Løken
AU  - Sheryl Palmero
AU  - Jørgen A. Gravning
AU  - Ivar Sjaastad
AU  - Ida G. Lunde
AU  - Mathis K. Stokke
AU  - Ragnhild Helseth
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Cardiovascular Medicine
DO  - 10.3389/fcvm.2026.1790767
UR  - https://www.frontiersin.org/articles/10.3389/fcvm.2026.1790767/full
AB  - Introduction: Ageing is an independent risk factor for cardiovascular disease (CVD). Preclinical models of ageing are needed to better understand human diseases. Telomere shortening is a critical process in cellular ageing and senescence. In humans, it is well-established that telomere shortening in circulating leukocytes is associated with CVD, however, whether this applies to common preclinical models remains disputable. We investigated leukocyte telomere length (LTL), cardiac telomere length (CTL), and age-related cardiac remodeling and functional decline in commonly used laboratory rats.  Methods: Sprague-Dawley rats ( n = 51) were euthanized at 3, 9, 16, or 24 months (mo), respectively. Cardiac function was assessed by echocardiography. Relative telomere length, mRNA levels of telomerase and signature genes involved in inflammation and fibrosis were quantified in circulating leukocytes and left ventricular tissue by quantitative or digital droplet PCR (qPCR or ddPCR, respectively).  Results: Rats with increasing chronological age (16/24 months compared to 9 months) exhibited cardiac hypertrophy and diastolic dysfunction, as evidenced by increased septal and posterior wall thickness, and elevated E/e’ ratio, and increased cardiac expression of central inflammatory ( Il6 ) and fibrotic ( Ctgf ) genes. Relative LTL and CTL remained unchanged across chronological age groups (LTL: 9 months 1.000 vs. 16 months 0.939 vs. 24 months 1.120, p = 0.37; and CTL: 9 months 1.000 vs. 16 months 1.021 vs. 24 months 0.897, p = 0.42). CTL and LTL did not correlate ( r = −0.027, p = 0.89). No association with cardiac dysfunction was observed, neither for LTL nor CTL.  Discussion: Laboratory rats of high age exhibited cardiac hypertrophy and dysfunction, resembling human cardiac ageing, however we found no evidence of shorter telomere lengths in circulating leukocytes nor cardiac cells, suggesting a translational gap.
SN  - 2297-055X
ER  -