ArticlePeerJ2025
UQCRC1 downregulation impairs cognitive function in mice
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Transcriptomic profiling and structural characterization reveal UQCRC1 and COX4I1 as key mitochondrial regulators associated with oxidative stress in multiple sclerosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) is an essential subunit of complex III in the mitochondrial respiratory chain. Although earlier studies have indicated that UQCRC1 downregulation causes cognitive impairment, the underlying mechanisms remain unclear. Methods: To investigate its pathophysiological effects, we developed a mouse model with downregulated UQCRC1 expression. Hippocampus-dependent cognitive performance was evaluated using a series of behavioral paradigms. Mitochondrial bioenergetic status was assessed by measuring adenosine triphosphate (ATP) levels, while oxidative stress was quantified through detection of reactive oxygen species (ROS). Molecular analyses were performed to assess AMP-activated protein kinase (AMPK) signaling dynamics and autophagic flux. Additionally, pharmacological interventions aimed at activating AMPK and enhancing lysosomal function were employed to elucidate mechanistic pathways. Results: Downregulation of UQCRC1 resulted in significant deficits in hippocampus-dependent cognitive performance, accompanied by impaired mitochondrial bioenergetics (lower ATP synthesis) and elevated oxidative stress (increased ROS levels). Mechanistically, these phenotypes were associated with diminished AMPK activation and disrupted autophagic flux. Importantly, pharmacological activation of AMPK or enhancement of lysosomal activity in UQCRC1-deficient mice effectively ameliorated cognitive deficits and restored mitochondrial redox homeostasis . Conclusions: This study identifies AMPK as a pivotal metabolic orchestrator of mitochondrial-lysosomal functional crosstalk and reveals its non-canonical function in maintaining neuronal homeostasis
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Registered trials
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