ArticleJournal of molecular medicine (Berlin, Germany)2017
S100A8/MYD88/NF-қB: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Serum S100A8/A9 Correlates to Surgery-Free Interval in Idiopathic Subglottic Stenosis.The Laryngoscope · 2025Article
- S100A8-CAMKK2-AMPK axis confers the protective effects of mild hypothermia against cerebral ischemia-reperfusion injury in rats.Scientific reports · 2025Article
- NF-κB-Specific Suppression in Cardiomyocytes Unveils Aging-Associated Responses in Cardiac Tissue.Biomedicines · 2025Article
- Lack of canonical thyroid hormone receptor α signaling changes regulatory T cell phenotype in female mice.iScience · 2024Article
- Cardiac hypertrophy that affects hyperthyroidism occurs independently of the NLRP3 inflammasome.Pflugers Archiv : European journal of physiology · 2024Article
- S100a8/A9 proteins: critical regulators of inflammation in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Glutamine supplementation accelerates functional recovery of EDL muscles after injury by modulating the expression of S100 calcium-binding proteins.Histochemistry and cell biology · 2023Article
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Circular RNA circ-RCCD promotes cardiomyocyte differentiation in mouse embryo development via recruiting YY1 to the promoter of MyD88.Journal of cellular and molecular medicine · 2022Article
- Review
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4.Frontiers in cardiovascular medicine · 2020Review
- Combined Signature of the Fecal Microbiome and Plasma Metabolome in Patients with Ulcerative Colitis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- AT1 receptor blockage impairs NF-κB activation mediated by thyroid hormone in cardiomyocytes.Pflugers Archiv : European journal of physiology · 2018Article
- Metabolic reprogramming via PPARα signaling in cardiac hypertrophy and failure: From metabolomics to epigenetics.American journal of physiology. Heart and circulatory physiology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have evidenced the involvement of inflammation-related pathways to the development of cardiac hypertrophy and other consequences on the cardiovascular system, including the calcium-binding protein S100A8. However, this has never been investigated in the thyroid hormone (TH)-prompted cardiac hypertrophy. Thus, we aimed to test whether S100A8 and related signaling molecules, myeloid differentiation factor-88 (MyD88) and nuclear factor kappa B (NF-қB), could be associated with the cardiomyocyte hypertrophy induced by TH. Our results demonstrate that the S100A8/MyD88/NF-қB signaling pathway is activated in cardiomyocytes following TH stimulation. The knockdown of S100A8 and MyD88 indicates the contribution of those molecules to cardiomyocyte hypertrophy in response to TH, as evaluated by cell surface area, leucine incorporation assay, and gene expression. Furthermore, S100A8 and MyD88 are crucial mediators of NF-қB activation, which is also involved in the hypertrophic growth of TH-treated cardiomyocytes. Supporting the in vitro data, the contribution of NF-қB for TH-induced cardiac hypertrophy is confirmed in vivo, by using transgenic mice with cardiomyocyte-specific suppression of NF-қB. These data identify a novel pathway regulated by TH that mediates cardiomyocyte hypertrophy. However, the potential role of this new pathway in short and long-term cardiac effects of TH remains to be further investigated. KEY MESSAGES: Inflammation-related signaling is activated by T3 in cardiomyocytes. S100A8 and MyD88 have a crucial role in cardiomyocyte hypertrophy by T3. S100A8 and MyD88 mediate NF-қB activation by T3. NF-қB contributes to T3-induced cardiac hypertrophy in vitro and in vivo.
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