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Abstract <p>In this work we investigated the rearrangements in the cristae structure and possible connection of these changes with the level of MICOS proteins in rat liver mitochondria in experimentally induced hyperthyroidism. A model of hyperthyroidism (HT) was induced by chronic administration of thyroxine. A change in the structure of liver mitochondria of hyperthyroid rats (HR) was found to consist of swollen organelles with a slightly altered number of cristae. A part of mitochondria (13%) in HR had vacuolized matrix with simultaneously reduced number of cristae. An increase in the protein levels of MIC 60, MIC 25, and MIC 19 was shown in the HT condition, while the quantity of MIC 10 was unchanged. In turn, the levels of SAMM 50 and OPA1 were reduced in HR. The data obtained indicate that excess thyroid hormones cause partial changes in the structure of liver mitochondria and reduce the content of SAMM50 and OPA1 proteins, which can be considered as possible targets for investigating therapeutic strategies for metabolic disorders associated with mitochondrial dysfunction.</p>

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The Role of Cristae Regulatory Proteins in Mitochondrial Dysfunction in an Experimentally Induced Hyperthyroidism Model

  • 期刊论文

  • 发表日期：

    2025年3月1日

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  • N. I. Venediktova,
  • I. N. Solomadin,
  • V. P. Medvedeva

摘要

Abstract

In this work we investigated the rearrangements in the cristae structure and possible connection of these changes with the level of MICOS proteins in rat liver mitochondria in experimentally induced hyperthyroidism. A model of hyperthyroidism (HT) was induced by chronic administration of thyroxine. A change in the structure of liver mitochondria of hyperthyroid rats (HR) was found to consist of swollen organelles with a slightly altered number of cristae. A part of mitochondria (13%) in HR had vacuolized matrix with simultaneously reduced number of cristae. An increase in the protein levels of MIC 60, MIC 25, and MIC 19 was shown in the HT condition, while the quantity of MIC 10 was unchanged. In turn, the levels of SAMM 50 and OPA1 were reduced in HR. The data obtained indicate that excess thyroid hormones cause partial changes in the structure of liver mitochondria and reduce the content of SAMM50 and OPA1 proteins, which can be considered as possible targets for investigating therapeutic strategies for metabolic disorders associated with mitochondrial dysfunction.