ArticleBiomedicines2022
Mitochondrial Ribosome Dysfunction in Human Alveolar Type II Cells in Emphysema.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Adenine nucleotide translocase 2 (ANT2) deficiency reprograms ferroptosis in alveolar progenitor cells to promote emphysema.bioRxiv : the preprint server for biology · 2026Article
- Exploring the diagnostic and immune infiltration roles of disulfidptosis related genes in pulmonary hypertension.Respiratory research · 2024Article
- Cellular and Molecular Biology of Mitochondria in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- Review
- Botanical formulation HX110B ameliorates PPE-induced emphysema in mice via regulation of PPAR/RXR signaling pathway.PloS one · 2024Article
- CD8 T cell response and its released cytokine IFN-γ are necessary for lung alveolar epithelial repair during bacterial pneumonia.Frontiers in immunology · 2023Article
- Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary emphysema is characterized by airspace enlargement and the destruction of alveoli. Alveolar type II (ATII) cells are very abundant in mitochondria. OXPHOS complexes are composed of proteins encoded by the mitochondrial and nuclear genomes. Mitochondrial 12S and 16S rRNAs are required to assemble the small and large subunits of the mitoribosome, respectively. We aimed to determine the mechanism of mitoribosome dysfunction in ATII cells in emphysema. ATII cells were isolated from control nonsmokers and smokers, and emphysema patients. Mitochondrial transcription and translation were analyzed. We also determined the miRNA expression. Decreases in ND1 and UQCRC2 expression levels were found in ATII cells in emphysema. Moreover, nuclear NDUFS1 and SDHB levels increased, and mitochondrial transcribed ND1 protein expression decreased. These results suggest an impairment of the nuclear and mitochondrial stoichiometry in this disease. We also detected low levels of the mitoribosome structural protein MRPL48 in ATII cells in emphysema. Decreased 16S rRNA expression and increased 12S rRNA levels were observed. Moreover, we analyzed miR4485-3p levels in this disease. Our results suggest a negative feedback loop between miR-4485-3p and 16S rRNA. The obtained results provide molecular mechanisms of mitoribosome dysfunction in ATII cells in emphysema.
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Registered trials
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