ArticleMolecular and cellular biology2012
Differential impairment of catecholaminergic cell maturation and survival by genetic mitochondrial complex II dysfunction.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Pathway coessentiality mapping reveals complex II is required for de novo purine biosynthesis in acute myeloid leukaemia.Nature metabolism · 2025Article
- Mouse developmental defects, but not paraganglioma tumorigenesis, upon conditional Complex II loss in early Sox10FASEB bioAdvances · 2024Article
- Article
- Succinate dehydrogenase complex subunit C: Role in cellular physiology and disease.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- The Adult Carotid Body: A Germinal Niche at the Service of Physiology.Advances in experimental medicine and biology · 2023Article
- Oxygen regulation of breathing is abolished in mitochondrial complex III-deficient arterial chemoreceptors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Succinate dehydrogenase/complex II is critical for metabolic and epigenetic regulation of T cell proliferation and inflammation.Science immunology · 2022Article
- SDHB knockout and succinate accumulation are insufficient for tumorigenesis but dual SDHB/NF1 loss yields SDHx-like pheochromocytomas.Cell reports · 2022Article
- Model systems in SDHx-related pheochromocytoma/paraganglioma.Cancer metastasis reviews · 2021Review
- Developmental role of PHD2 in the pathogenesis of pseudohypoxic pheochromocytoma.Endocrine-related cancer · 2021Article
- Unexpected obesity, rather than tumorigenesis, in a conditional mouse model of mitochondrial complex II deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Pheochromocytoma/paraganglioma preclinical models: which to use and why?Endocrine connections · 2020Review
- Molecular Mechanisms of Acute Oxygen Sensing by Arterial Chemoreceptor Cells. Role of Hif2α.Frontiers in physiology · 2020Review
- The carotid body: a physiologically relevant germinal niche in the adult peripheral nervous system.Cellular and molecular life sciences : CMLS · 2019Review
- Substantia nigra dopaminergic neurons and striatal interneurons are engaged in three parallel but interdependent postnatal neurotrophic circuits.Aging cell · 2018Article
- Metabolic implications of hypoxia and pseudohypoxia in pheochromocytoma and paraganglioma.Cell and tissue research · 2018Review
- Oxygen sensing and stem cell activation in the hypoxic carotid body.Cell and tissue research · 2018Review
- Rodent models of pheochromocytoma, parallels in rodent and human tumorigenesis.Cell and tissue research · 2018Review
- Gene expression analyses reveal metabolic specifications in acute OThe Journal of physiology · 2017Article
- Redox signaling in acute oxygen sensing.Redox biology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SDHD gene (subunit D of succinate dehydrogenase) has been shown to be involved in the generation of paragangliomas and pheochromocytomas. Loss of heterozygosity of the normal allele is necessary for tumor transformation of the affected cells. As complete SdhD deletion is lethal, we have generated mouse models carrying a "floxed" SdhD allele and either an inducible (SDHD-ESR strain) or a catecholaminergic tissue-specific (TH-SDHD strain) CRE recombinase. Ablation of both SdhD alleles in adult SDHD-ESR mice did not result in generation of paragangliomas or pheochromocytomas. In contrast, carotid bodies from these animals showed smaller volume than controls. In accord with these observations, the TH-SDHD mice had decreased cell numbers in the adrenal medulla, carotid body, and superior cervical ganglion. They also manifested inhibited postnatal maturation of mesencephalic dopaminergic neurons and progressive cell loss during the first year of life. These alterations were particularly intense in the substantia nigra, the most affected neuronal population in Parkinson's disease. Unexpectedly, TH(+) neurons in the locus coeruleus and group A13, also lacking the SdhD gene, were unaltered. These data indicate that complete loss of SdhD is not sufficient to induce tumorigenesis in mice. They suggest that substantia nigra neurons are more susceptible to mitochondrial damage than other catecholaminergic cells, particularly during a critical postnatal maturation period.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.