ArticleCurrent research in physiology2023
Physiological levels of cardiolipin acutely affect mitochondrial respiration in vascular smooth muscle cells.
Article in Current research in physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Mitochondrial Functional Capacity Is Impaired in Angiotensin II-Infused Mice and Not Recovered by Metformin.Biomedicines · 2026Article
- Intraperitoneal Administration of Cardiolipin Enhances Mitochondrial Respiration in Skeletal Muscle of Male Mice.Journal of experimental pharmacology · 2026Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Cardiolipin (CL) is a phospholipid molecule found in the inner mitochondrial membrane, where it normally associates with and activates the respiratory complexes. Following myocardial infarction, CL gets released from necrotic cells, consequently affecting neighboring tissues. We have previously demonstrated that physiological concentrations of up to 100 μM CL diminish endothelial cell migration and angiogenic sprouting. Since CL is vital to cellular life, we hypothesized that this molecule may have considerable implications on vascular smooth muscle cells bioenergetics, a key phase in atherogenesis. We examined the acute effects of physiological concentrations of CL on oxidative phosphorylation in permeabilized mice aorta using high-resolution respirometry and a substrate-inhibitor titration protocol. We found that CL significantly lowers LEAK and maximal State 3 respiration. In addition, we found that the acceptor control ratio, representing the coupling between oxidation and phosphorylation, was significantly upregulated by CL. Our findings demonstrate that
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