Cardiomyocyte and endothelial cells play distinct roles in the tumour necrosis factor (TNF)-dependent atrial responses and increased atrial fibrillation vulnerability induced by endurance exercise training in mice Article Swipe
Robert Lakin
,
Nazari Polidovitch
,
Sibao Yang
,
Mihir Parikh
,
Xueyan Liu
,
Ryan Debi
,
Xiao‐Dong Gao
,
Wenliang Chen
,
Camilo Guzmán
,
Simona Yakobov
,
Farzad Izaddoustdar
,
Marianne Wauchop
,
Qian Lei
,
Weimin Xu
,
Sergei A. Nedospasov
,
Vincent M. Christoffels
,
Peter H. Backx
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/cvr/cvad144
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1093/cvr/cvad144
Aims Endurance exercise is associated with an increased risk of atrial fibrillation (AF). We previously established that adverse atrial remodelling and AF susceptibility induced by intense exercise in mice require the mechanosensitive and pro-inflammatory cytokine tumour necrosis factor (TNF). The cellular and mechanistic basis for these TNF-mediated effects is unknown. Methods and results We studied the impact of Tnf excision, in either atrial cardiomyocytes or endothelial cells (using Cre-recombinase expression controlled by Nppa or Tie2 promoters, respectively), on the cardiac responses to six weeks of intense swim exercise training. TNF ablation, in either cell type, had no impact on the changes in heart rate, autonomic tone, or left ventricular structure and function induced by exercise training. Tnf excision in atrial cardiomyocytes did, however, prevent atrial hypertrophy, fibrosis, and macrophage infiltration as well as conduction slowing and increased AF susceptibility arising from exercise training. In contrast, endothelial-specific excision only reduced the training-induced atrial hypertrophy. Consistent with these cell-specific effects of Tnf excision, inducing TNF loss from atrial cardiomyocytes prevented activation of p38MAPKinase, a strain-dependent downstream mediator of TNF signalling, without affecting the atrial stretch as assessed by atrial pressures induced by exercise. Despite TNF’s established role in innate immune responses and inflammation, neither acute nor chronic exercise training caused measurable NLRP3 inflammasome activation. Conclusions Our findings demonstrate that adverse atrial remodelling and AF vulnerability induced by intense exercise require TNF in atrial cardiomyocytes whereas the impact of endothelial-derived TNF is limited to hypertrophy modulation. The implications of the cell autonomous effects of TNF and crosstalk between cells in the atria are discussed.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/cvr/cvad144
- OA Status
- green
- Cited By
- 20
- References
- 56
- Related Works
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- OpenAlex ID
- https://openalex.org/W4386793927
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4386793927Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1093/cvr/cvad144Digital Object Identifier
- Title
-
Cardiomyocyte and endothelial cells play distinct roles in the tumour necrosis factor (TNF)-dependent atrial responses and increased atrial fibrillation vulnerability induced by endurance exercise training in miceWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-09-14Full publication date if available
- Authors
-
Robert Lakin, Nazari Polidovitch, Sibao Yang, Mihir Parikh, Xueyan Liu, Ryan Debi, Xiao‐Dong Gao, Wenliang Chen, Camilo Guzmán, Simona Yakobov, Farzad Izaddoustdar, Marianne Wauchop, Qian Lei, Weimin Xu, Sergei A. Nedospasov, Vincent M. Christoffels, Peter H. BackxList of authors in order
- Landing page
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https://doi.org/10.1093/cvr/cvad144Publisher landing page
- Open access
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YesWhether a free full text is available
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-
greenOpen access status per OpenAlex
- OA URL
-
https://pmc.ncbi.nlm.nih.gov/articles/PMC10730243/pdf/cvad144.pdfDirect OA link when available
- Concepts
-
Medicine, Internal medicine, Tumor necrosis factor alpha, Atrial fibrillation, Inflammation, Muscle hypertrophy, Fibrosis, Endocrinology, Endurance training, Cytokine, CardiologyTop concepts (fields/topics) attached by OpenAlex
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20Total citation count in OpenAlex
- Citations by year (recent)
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2025: 10, 2024: 9, 2023: 1Per-year citation counts (last 5 years)
- References (count)
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56Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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