ReviewJournal of inherited metabolic disease2024
Pathological variants in nuclear genes causing mitochondrial complex III deficiency: An update.
Review in Journal of inherited metabolic disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- TEX44 deficiency induces asthenoteratozoospermia by disrupting sperm axonemal integrity and mitochondrial sheath assembly, and ICSI enables successful fertility rescue.Journal of assisted reproduction and genetics · 2026Article
- Mitochondrial Collapse Responsible for Chagasic and Post-Ischemic Heart Failure Is Reversed by Cell Therapy Under Different Transcriptomic Topologies.Current issues in molecular biology · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
- Pathological variants in nuclear genes causing mitochondrial complex III deficiency: An update.Journal of inherited metabolic disease · 2024Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Mitochondrial disorders are a group of clinically and biochemically heterogeneous genetic diseases within the group of inborn errors of metabolism. Primary mitochondrial diseases are mainly caused by defects in one or several components of the oxidative phosphorylation system (complexes I-V). Within these disorders, those associated with complex III deficiencies are the least common. However, thanks to a deeper knowledge about complex III biogenesis, improved clinical diagnosis and the implementation of next-generation sequencing techniques, the number of pathological variants identified in nuclear genes causing complex III deficiency has expanded significantly. This updated review summarizes the current knowledge concerning the genetic basis of complex III deficiency, and the main clinical features associated with these conditions.
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