ArticleClinical and translational medicine2022
LncRNA LOC105378097 inhibits cardiac mitophagy in natural ageing mice.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Decoding noncoding RNAs in regulating cardiovascular aging and age-related conditions: the emerging landscape.Science China. Life sciences · 2026Review
- Cardiomyocyte-specific long noncoding RNA Trdn-as induces mitochondrial calcium overload by promoting the mFrontiers of medicine · 2025Article
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- MiR-203 improves cardiac dysfunction by targeting PARP1-NADAging cell · 2024Article
- Unlocking the dark matter: noncoding RNAs and RNA modifications in cardiac aging.American journal of physiology. Heart and circulatory physiology · 2024Review
- Review
- Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression.Frontiers in immunology · 2024Review
- Mitophagy-related long non-coding RNA signature predicts prognosis and drug response in Ovarian Cancer.Journal of ovarian research · 2023Article
- Metabolic Changes in Cardiac Aging.Reviews in cardiovascular medicine · 2023Review
- LncRNA LOC105378097 inhibits cardiac mitophagy in natural ageing mice.Clinical and translational medicine · 2022Article
- Article
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Authors and funding
20 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe development of heart ageing is the main cause of chronic disability, disease and death in the elderly. Ample evidence has established a pivotal role for significantly reduced mitophagy in the ageing heart. However, the underlying mechanisms of mitophagy deficiency in ageing heart are little known. The present study aimed to explore the underlying mechanisms of lncRNA LOC105378097 (Senescence-Mitophagy Associated LncRNA, lncR-SMAL) actions on mitophagy in the setting of heart ageing.
methodsThe expression of lncR-SMAL was measured in serum from different ages of human and heart from different ages of mice through a quantitative real-time polymerase chain reaction. The effects of lncR-SMAL on heart function of mice were assessed by echocardiography and pressure-volume measurements system. Cardiac senescence was evaluated by hematoxylin-eosin staining, senescence-associated β-galactosidase staining, flow cytometry and western blot analysis of expression of ageing related markes p53 and p21. Cardiomyocyte mitophagy was assessed by western blot, mRFP-GFP-LC3 adenovirus particles transfection and mito-Keima staining. Interaction between lncR-SMAL and Parkin was validated through molecular docking, RNA immunoprecipitation (RIP) and RNA pull-down assay. Ubiquitination assay was performed to explore the molecular mechanism of Parkin inhibition. The effects of lncR-SMAL on mitochondrial function were investigated through electron microscopic examination, JC-1 staining and oxygen consumption rates analysis.
resultsThe heart-enriched lncR-SMAL reached the expression crest in the serum of human at an age of 60. Exogenously overexpression of lncRNA SMAL deteriorated cardiac function exactly as natural ageing and inhibited the associated cardiomyocytes mitophagy by depressing Parkin protein level. Improved heart ageing and mitophagy caused by Parkin overexpression were reversed by lncR-SMAL in mice. In contrast, the loss of lncR-SMAL in AC16 cells induced the upregulation of Parkin protein and ameliorated mitophagy and mitochondrial dysfunction, resulting in alleviated cardiac senescence. Besides, we found the interaction between lncR-SMAL and Parkin protein through computational docking analysis, pull-down and RIP assay. This would contribute to the promotive effect of lncR-SMAL on Parkin ubiquitination and decrease Parkin protein stability.
conclusionsThe present study for the first time demonstrates a heart-enriched lncRNA, SMAL, that inhibits the mitophagy of cardiomyocytes via the downregulation of Parkin protein, which further contributes to heart ageing and cardiac dysfunction in natural ageing mice.
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