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Peer-reviewedCC BY 4.0PLOS One

Cardiomyocyte hypertrophy co-localizes with accumulation of hyaluronan in cMyBPC+/- mice hearts

  • Anna Strnadová1
  • Madelene Ericsson2
  • Rakel Nyrén3
  • Ilona Dudka4
  • Stellan Mörner5
  • Urban Hellman
5 affiliations
  1. 1Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
  2. 2Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden
  3. 3Umeå Centre for Molecular Medicine, Umeå University, Umeå, Sweden
  4. 4Department of Chemistry, Umeå University, Umeå, Sweden
  5. 5Department of Clinical Microbiology, Umeå University, Umeå, Sweden
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Abstract

Hypertrophic cardiomyopathy (HCM) is a genetic heart disease characterized by left ventricular hypertrophy. Mutations in genes for sarcomere proteins, e.g., in cardiac myosin-binding protein C (cMyBPC), may cause symptoms like heart failure and sudden cardiac death. In HCM, the heart utilizes high amounts of glucose. Increased glucose metabolism creates intermediates for hyaluronan (HA) synthesis, resulting in HA accumulation within the extracellular space, which could contribute to cardiomyocyte hypertrophy. We aimed to describe the connection between HA and cardiomyocyte hypertrophy using cMyBPC+/- mice treated with two different β-blockers – either metoprolol or propranolol – for 11 months. The results showed that HA metabolism is altered in HCM, and that HA is significantly more abundant in hearts of cMyBPC+/- mice compared to wild-type mice. Areas of high HA abundance were spread around the tissue in a ‘patchy’ manner. This focally increased HA concentration correlated with increased cardiomyocyte size in the same areas of the heart. Gene expression of HA synthase 2 was elevated in cMyBPC+/- mice. Treatment with propranolol maintained HA synthase 2 at wild-type level, while significantly increasing HA synthase 3 expression. However, treatment with metoprolol or propranolol did not prevent HA accumulation nor decreased cardiomyocyte hypertrophy. These novel findings visualise a spatial connection between high HA abundance and cardiomyocyte hypertrophy in the hearts of cMyBPC+/- mice.

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Cite

BibTeXRIS
BibTeX
@article{strnadova2026cardiomyocyte,
  title = {{Cardiomyocyte hypertrophy co-localizes with accumulation of hyaluronan in cMyBPC+/- mice hearts}},
  author = {Anna Strnadová and Madelene Ericsson and Rakel Nyrén and Ilona Dudka and Stellan Mörner and Urban Hellman},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0342635},
  url = {https://doi.org/10.1371/journal.pone.0342635},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Cardiomyocyte hypertrophy co-localizes with accumulation of hyaluronan in cMyBPC+/- mice hearts
AU  - Anna Strnadová
AU  - Madelene Ericsson
AU  - Rakel Nyrén
AU  - Ilona Dudka
AU  - Stellan Mörner
AU  - Urban Hellman
PY  - 2026
DA  - 2026/09/09
JO  - PLOS One
DO  - 10.1371/journal.pone.0342635
UR  - https://doi.org/10.1371/journal.pone.0342635
AB  - Hypertrophic cardiomyopathy (HCM) is a genetic heart disease characterized by left ventricular hypertrophy. Mutations in genes for sarcomere proteins, e.g., in cardiac myosin-binding protein C (cMyBPC), may cause symptoms like heart failure and sudden cardiac death. In HCM, the heart utilizes high amounts of glucose. Increased glucose metabolism creates intermediates for hyaluronan (HA) synthesis, resulting in HA accumulation within the extracellular space, which could contribute to cardiomyocyte hypertrophy. We aimed to describe the connection between HA and cardiomyocyte hypertrophy using cMyBPC+/- mice treated with two different β-blockers – either metoprolol or propranolol – for 11 months. The results showed that HA metabolism is altered in HCM, and that HA is significantly more abundant in hearts of cMyBPC+/- mice compared to wild-type mice. Areas of high HA abundance were spread around the tissue in a ‘patchy’ manner. This focally increased HA concentration correlated with increased cardiomyocyte size in the same areas of the heart. Gene expression of HA synthase 2 was elevated in cMyBPC+/- mice. Treatment with propranolol maintained HA synthase 2 at wild-type level, while significantly increasing HA synthase 3 expression. However, treatment with metoprolol or propranolol did not prevent HA accumulation nor decreased cardiomyocyte hypertrophy. These novel findings visualise a spatial connection between high HA abundance and cardiomyocyte hypertrophy in the hearts of cMyBPC+/- mice.
SN  - 1932-6203
ER  -