ArticleAmerican journal of physiology. Endocrinology and metabolism2026
Skeletal muscle carnitine-acylcarnitine translocase deletion reveals vulnerability of oxidative muscle to fatty acid oxidation deficiency.
Article in American journal of physiology. Endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Analysis of Differences in Flavor Precursors Between Fast and Slow Muscles of Turpan Black Sheep Based on Lipidomics and Proteomics.Foods (Basel, Switzerland) · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Fatty acid oxidation (FAO) is a critical bioenergetic source for skeletal muscle, with FAO impairments being linked to metabolic and contractile dysfunction. FAO is regulated by the carnitine shuttle, in which FAO-eligible fatty acids, in the form of acylcarnitines, are transported into the mitochondrial matrix by carnitine-acylcarnitine translocase (CACT); however, the role of CACT in muscle in vivo has remained unexplored. To determine the requirement of CACT in muscle FAO and its influence on muscle mitochondrial bioenergetics, lipid profile, and muscle contractility, a novel conditional skeletal muscle-specific CACT knockout mouse (
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