Mitochondrial Complex V Deficiency Latest Advances
Find the Latest Research About Mitochondrial Complex V Deficiency
Last Updated: 09/19/2026
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Found 308 publications
LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.
Journal: Circulation research
Published: May 27, 2026
LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.
Journal: Circulation research
Published: May 27, 2026
Multi-generational mitochondrial complex V deficiency due to the recurrent ATP5F1A c.620G>A (p.Arg207His) pathogenic variant: A novel family and a review of the literature.
Journal: Molecular genetics and metabolism
Published: April 20, 2026
Decreased plasma citrulline is a biochemical marker in newborn screening for MT-ATP6-associated mitochondrial disease: two case reports and a literature review
Journal: Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
Published: March 02, 2026
Generative AI Accelerates Genotype-Phenotype Characterization of a 1600-Case Leigh Syndrome Virtual Cohort from Published Literature.
Journal: Biology
Published: December 27, 2025
Biallelic Loss-Of-Function Variant in ATP5ME Is Associated With Severe and Early Onset Oxidative Phosphorylation Deficiency.
Journal: Journal of inherited metabolic disease
Published: December 05, 2025
Lysosomal storage, mitochondrial pathology, and autophagy in knockout of tripeptidyl peptidase 1 in human neuroblastoma cells in vitro.
Journal: Molecular genetics and metabolism
Published: December 04, 2025
Sex, stress, and the heart: long-term cardiovascular effects of embryonic metabolic disruption.
Journal: American journal of physiology. Heart and circulatory physiology
Published: November 26, 2025
Clinical utility of the ATP hydrolysis assay for the diagnosis of complex V deficiency in cultured skin fibroblasts.
Journal: Molecular genetics and metabolism
Published: August 20, 2025
Dominant negative ATP5F1A variants disrupt oxidative phosphorylation causing neurological disorders.
Dominant negative ATP5F1A variants disrupt oxidative phosphorylation causing neurological disorders.
Journal: medRxiv : the preprint server for health sciences
Published: July 17, 2025
Downregulation of LATS1/2 Drives Endothelial Senescence-Associated Stemness (SAS) and Atherothrombotic Lesion Formation.
Journal: bioRxiv : the preprint server for biology
Published: July 16, 2025
Nicotinamide nucleotide transhydrogenase dysfunction transcriptionally impacts mitochondrial β-oxidation and neuromuscular junction in M. Gastrocnemius of 24-day-old mice.
Journal: International journal of biological macromolecules
Published: July 09, 2025
Last Updated: 09/19/2026