Katalog Plus
Bibliothek der Frankfurt UAS
Bald neuer Katalog: sichern Sie sich schon vorab Ihre persönlichen Merklisten im Nutzerkonto: Anleitung.
Dieses Ergebnis aus BASE kann Gästen nicht angezeigt werden.  Login für vollen Zugriff.

Imbalance in MICOS Proteins in Rat Liver Mitochondria in an Induced Hyperthyroidism Model

Title: Imbalance in MICOS Proteins in Rat Liver Mitochondria in an Induced Hyperthyroidism Model
Authors: Natalya Venediktova; Ilya Solomadin; Anna Nikiforova; Tatiana Bessonova
Source: Cells ; Volume 14 ; Issue 23 ; Pages: 1877
Publisher Information: Multidisciplinary Digital Publishing Institute
Publication Year: 2025
Collection: MDPI Open Access Publishing
Subject Terms: cristae membranes; hyperthyroidism; MICOS; OPA1; cardiolipin; oxidative phosphorylation; calcium retention capacity
Description: This study investigated rearrangements in the cristae structure and the possible relationship between these changes and the MICOS levels in the liver mitochondria of rats with experimentally induced hyperthyroidism. In hyperthyroid rats (HRs), the number, area, and perimeter of mitochondria were increased, and organelles of a worm-shaped, branched, highly elongated, or spherical shape appeared. A structural change in the mitochondria of HR liver was detected, consisting of a decrease in the number of cristae relative to the cross-section of the organelle. In some mitochondria, multilamellar bodies were detected. Hyperthyroidism caused an increase in the expression of genes and the level of proteins of the MIC60 subcomplex, with an unchanged level of the MIC10 subcomplex. Moreover, the levels of Sam50 and OPA1 in HRs were reduced. A functional assessment of HR mitochondria revealed changes in oxygen consumption, a decrease in membrane potential, and disruption of Ca2+ homeostasis. These data indicate that excess thyroid hormones cause partial changes in liver mitochondrial structure and an imbalance in the levels of Mic60 and Mic10 subcomplex proteins. The decreased levels of Sam50 and OPA1 proteins suggest their potential as targets for correcting mitochondrial dysfunction in metabolic disorders.
Document Type: text
File Description: application/pdf
Language: English
Relation: https://dx.doi.org/10.3390/cells14231877
DOI: 10.3390/cells14231877
Availability: https://doi.org/10.3390/cells14231877
Rights: https://creativecommons.org/licenses/by/4.0/
Accession Number: edsbas.F83B990B
Database: BASE