Thyroid Hormone Action in Muscle Atrophy
Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to su...
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oai:doaj.org-article:c7c8c086f38c414facbf475426fd81e82021-11-25T18:20:30ZThyroid Hormone Action in Muscle Atrophy10.3390/metabo111107302218-1989https://doaj.org/article/c7c8c086f38c414facbf475426fd81e82021-10-01T00:00:00Zhttps://www.mdpi.com/2218-1989/11/11/730https://doaj.org/toc/2218-1989Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to substantial muscle mass loss and weakness. Muscle protein breakdown reflects the activation of multiple proteolytic mechanisms, including lysosomal degradation, apoptosis, and ubiquitin–proteasome. Thyroid hormone (TH) plays a key role in these conditions. Indeed, skeletal muscle is among the principal TH target tissue, where TH regulates proliferation, metabolism, differentiation, homeostasis, and growth. In physiological conditions, TH stimulates both protein synthesis and degradation, and an alteration in TH levels is often responsible for a specific myopathy. Intracellular TH concentrations are modulated in skeletal muscle by a family of enzymes named deiodinases; in particular, in muscle, deiodinases type 2 (D2) and type 3 (D3) are both present. D2 activates the prohormone T4 into the active form triiodothyronine (T3), whereas D3 inactivates both T4 and T3 by the removal of an inner ring iodine. Here we will review the present knowledge of TH action in skeletal muscle atrophy, in particular, on the molecular mechanisms presiding over the control of intracellular T3 concentration in wasting muscle conditions. Finally, we will discuss the possibility of exploiting the modulation of deiodinases as a possible therapeutic approach to treat muscle atrophy.Maria Angela De StefanoRaffaele AmbrosioTommaso PorcelliGianfranco OrlandinoDomenico SalvatoreCristina LuongoMDPI AGarticlethyroid hormonedeiodinasemuscle atrophyMicrobiologyQR1-502ENMetabolites, Vol 11, Iss 730, p 730 (2021) |
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thyroid hormone deiodinase muscle atrophy Microbiology QR1-502 |
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thyroid hormone deiodinase muscle atrophy Microbiology QR1-502 Maria Angela De Stefano Raffaele Ambrosio Tommaso Porcelli Gianfranco Orlandino Domenico Salvatore Cristina Luongo Thyroid Hormone Action in Muscle Atrophy |
description |
Skeletal muscle atrophy is a condition associated with various physiological and pathophysiological conditions, such as denervation, cachexia, and fasting. It is characterized by an altered protein turnover in which the rate of protein degradation exceeds the rate of protein synthesis, leading to substantial muscle mass loss and weakness. Muscle protein breakdown reflects the activation of multiple proteolytic mechanisms, including lysosomal degradation, apoptosis, and ubiquitin–proteasome. Thyroid hormone (TH) plays a key role in these conditions. Indeed, skeletal muscle is among the principal TH target tissue, where TH regulates proliferation, metabolism, differentiation, homeostasis, and growth. In physiological conditions, TH stimulates both protein synthesis and degradation, and an alteration in TH levels is often responsible for a specific myopathy. Intracellular TH concentrations are modulated in skeletal muscle by a family of enzymes named deiodinases; in particular, in muscle, deiodinases type 2 (D2) and type 3 (D3) are both present. D2 activates the prohormone T4 into the active form triiodothyronine (T3), whereas D3 inactivates both T4 and T3 by the removal of an inner ring iodine. Here we will review the present knowledge of TH action in skeletal muscle atrophy, in particular, on the molecular mechanisms presiding over the control of intracellular T3 concentration in wasting muscle conditions. Finally, we will discuss the possibility of exploiting the modulation of deiodinases as a possible therapeutic approach to treat muscle atrophy. |
format |
article |
author |
Maria Angela De Stefano Raffaele Ambrosio Tommaso Porcelli Gianfranco Orlandino Domenico Salvatore Cristina Luongo |
author_facet |
Maria Angela De Stefano Raffaele Ambrosio Tommaso Porcelli Gianfranco Orlandino Domenico Salvatore Cristina Luongo |
author_sort |
Maria Angela De Stefano |
title |
Thyroid Hormone Action in Muscle Atrophy |
title_short |
Thyroid Hormone Action in Muscle Atrophy |
title_full |
Thyroid Hormone Action in Muscle Atrophy |
title_fullStr |
Thyroid Hormone Action in Muscle Atrophy |
title_full_unstemmed |
Thyroid Hormone Action in Muscle Atrophy |
title_sort |
thyroid hormone action in muscle atrophy |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/c7c8c086f38c414facbf475426fd81e8 |
work_keys_str_mv |
AT mariaangeladestefano thyroidhormoneactioninmuscleatrophy AT raffaeleambrosio thyroidhormoneactioninmuscleatrophy AT tommasoporcelli thyroidhormoneactioninmuscleatrophy AT gianfrancoorlandino thyroidhormoneactioninmuscleatrophy AT domenicosalvatore thyroidhormoneactioninmuscleatrophy AT cristinaluongo thyroidhormoneactioninmuscleatrophy |
_version_ |
1718411345960894464 |