ArticlePloS one2019
Modeling succinate dehydrogenase loss disorders in C. elegans through effects on hypoxia-inducible factor.
Article in PloS one, 2019. 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, 6 citations in OpenAlex.
- Approaches to reduce succinate accumulation by restoration of succinate dehydrogenase activity in cultured adrenal cells.Journal of cell science · 2025Article
- Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels inAntioxidants (Basel, Switzerland) · 2025Review
- The egg-counter: a novel microfluidic platform for characterization ofLab on a chip · 2024Article
- A suppressor of dioxygenase inhibition in a yeast model of SDH deficiency.Endocrine-related cancer · 2022Article
- Model systems in SDHx-related pheochromocytoma/paraganglioma.Cancer metastasis reviews · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial disorders arise from defects in nuclear genes encoding enzymes of oxidative metabolism. Mutations of metabolic enzymes in somatic tissues can cause cancers due to oncometabolite accumulation. Paraganglioma and pheochromocytoma are examples, whose etiology and therapy are complicated by the absence of representative cell lines or animal models. These tumors can be driven by loss of the tricarboxylic acid cycle enzyme succinate dehydrogenase. We exploit the relationship between succinate accumulation, hypoxic signaling, egg-laying behavior, and morphology in C. elegans to create genetic and pharmacological models of succinate dehydrogenase loss disorders. With optimization, these models may enable future high-throughput screening efforts.
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Registered trials
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