Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Dec 21;23(1):45. doi: 10.3390/ijms23010045

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Mitochondrial respiration rate (A) and flux control factors (B) in cardiac fibers of the left ventricle after administration of meldonium at a dose of 100 mg/kg for 3 weeks in a model of lipopolysaccharide (LPS)-induced left ventricle dysfunction. LPS induced the inhibition of fatty acid (FA)-dependent oxidative phosphorylation (A,B) and subsequently increased pyruvate metabolism (B). Treatment with meldonium fully restored mitochondrial bioenergetics (A,B) to the level of the normal control group. The results are presented as the mean±SEM of 9 animals. * p < 0.05 vs. the LPS group, one-way ANOVA with Dunnett’s multiple comparison test. Flux control factor, the contribution of each substrate/pathway to the respiration rate; p, pyruvate; S, succinate; F, FA oxidation-dependent pathway; N, NADH pathway; LEAK, substrate-dependent state; OXPHOS, oxidative phosphorylation-dependent state; ROX, residual oxygen consumption.

Mitochondrial respiration rate (A) and flux control factors (B) in cardiac fibers of the left ventricle after administration of meldonium at a dose of 100 mg/kg for 3 weeks in a model of lipopolysaccharide (LPS)-induced left ventricle dysfunction. LPS induced the inhibition of fatty acid (FA)-dependent oxidative phosphorylation (A,B) and subsequently increased pyruvate metabolism (B). Treatment with meldonium fully restored mitochondrial bioenergetics (A,B) to the level of the normal control group. The results are presented as the mean±SEM of 9 animals. * p < 0.05 vs. the LPS group, one-way ANOVA with Dunnett’s multiple comparison test. Flux control factor, the contribution of each substrate/pathway to the respiration rate; p, pyruvate; S, succinate; F, FA oxidation-dependent pathway; N, NADH pathway; LEAK, substrate-dependent state; OXPHOS, oxidative phosphorylation-dependent state; ROX, residual oxygen consumption.