ArticleScientific reports2020
DUSP5 expression in left ventricular cardiomyocytes of young hearts regulates thyroid hormone (T3)-induced proliferative ERK1/2 signaling.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Effect of levothyroxine replacement therapy in patients with subclinical hypothyroidism and chronic heart failure: A systematic review.Frontiers in endocrinology · 2022Pooled it
- Cardiac Endocrine Function and Hormonal Interplay in Pediatrics: From Development to Clinical Implications.Biomedicines · 2025Review
- Triiodothyronine protects infarcted myocardium by reducing apoptosis and preserving mitochondria.Basic research in cardiology · 2025Article
- Unravelling the Interplay between Cardiac Metabolism and Heart Regeneration.International journal of molecular sciences · 2023Review
- Redifferentiated cardiomyocytes retain residual dedifferentiation signatures and are protected against ischemic injury.Nature cardiovascular research · 2023Article
- Remuscularization with triiodothyronine and βScientific reports · 2022Article
- Nucleosome proteostasis and histone turnover.Frontiers in molecular biosciences · 2022Review
- The Insulin-like Growth Factor Signalling Pathway in Cardiac Development and Regeneration.International journal of molecular sciences · 2021Review
- Endocrine Influence on Cardiac Metabolism in Development and Regeneration.Endocrinology · 2021Review
- Thyroid Hormone Plays an Important Role in Cardiac Function: From Bench to Bedside.Frontiers in physiology · 2021Review
- Mechanism-Based Cardiac Regeneration Strategies in Mammals.Frontiers in cell and developmental biology · 2021Review
- Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiomyocytes of newborn mice proliferate after injury or exposure to growth factors. However, these responses are diminished after postnatal day-6 (P6), representing a barrier to building new cardiac muscle in adults. We have previously shown that exogenous thyroid hormone (T3) stimulates cardiomyocyte proliferation in P2 cardiomyocytes, by activating insulin-like growth factor-1 receptor (IGF-1R)-mediated ERK1/2 signaling. But whether exogenous T3 functions as a mitogen in post-P6 murine hearts is not known. Here, we show that exogenous T3 increases the cardiomyocyte endowment of P8 hearts, but the proliferative response is confined to cardiomyocytes of the left ventricular (LV) apex. Exogenous T3 stimulates proliferative ERK1/2 signaling in apical cardiomyocytes, but not in those of the LV base, which is inhibited by expression of the nuclear phospho-ERK1/2-specific dual-specificity phosphatase, DUSP5. Developmentally, between P7 and P14, DUSP5 expression increases in the myocardium from the LV base to its apex; after this period, it is uniformly expressed throughout the LV. In young adult hearts, exogenous T3 increases cardiomyocyte numbers after DUSP5 depletion, which might be useful for eliciting cardiac regeneration.
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Registered trials
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