ArticlePloS one2018
The effect of Tmem135 overexpression on the mouse heart.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Mitofusins are required for specialized mitochondrial morphology and function of rod photoreceptor cells.Frontiers in cell and developmental biology · 2026Article
- Mitochondrial Structure and Function in Human Heart Failure.Circulation research · 2024Review
- Connection Between HIV and Mitochondria in Cardiovascular Disease and Implications for Treatments.Circulation research · 2024Review
- The peroxisome: an update on mysteries 3.0.Histochemistry and cell biology · 2024Review
- Roles of transmembrane protein 135 in mitochondrial and peroxisomal functions - implications for age-related retinal disease.Frontiers in ophthalmology · 2024Article
- TMEM135 links peroxisomes to the regulation of brown fat mitochondrial fission and energy homeostasis.Nature communications · 2023Article
- Impact of Senolytic Treatment on Gene Expression in Aged Lung.International journal of molecular sciences · 2023Article
- Transmembrane protein 135 regulates lipid homeostasis through its role in peroxisomal DHA metabolism.Communications biology · 2023Article
- Cavβ1 regulates T cell expansion and apoptosis independently of voltage-gated CaNature communications · 2022Article
- A mutation in transmembrane protein 135 impairs lipid metabolism in mouse eyecups.Scientific reports · 2022Article
- Review
- Review
- Metabolic alterations caused by the mutation and overexpression of theExperimental biology and medicine (Maywood, N.J.) · 2020Article
- Modulation of Tmem135 Leads to Retinal Pigmented Epithelium Pathologies in Mice.Investigative ophthalmology & visual science · 2020Article
- Recent Insights Into SREBP as a Direct Mediator of Kidney Fibrosis via Lipid-Independent Pathways.Frontiers in pharmacology · 2020Review
- Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging.Oxidative medicine and cellular longevity · 2019Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Tissues with high-energy demand including the heart are rich in the energy-producing organelles, mitochondria, and sensitive to mitochondrial dysfunction. While alterations in mitochondrial function are increasingly recognized in cardiovascular diseases, the molecular mechanisms through which changes in mitochondria lead to heart abnormalities have not been fully elucidated. Here, we report that transgenic mice overexpressing a novel regulator of mitochondrial dynamics, transmembrane protein 135 (Tmem135), exhibit increased fragmentation of mitochondria and disease phenotypes in the heart including collagen accumulation and hypertrophy. The gene expression analysis showed that genes associated with ER stress and unfolded protein response, and especially the pathway involving activating transcription factor 4, are upregulated in the heart of Tmem135 transgenic mice. It also showed that gene expression changes in the heart of Tmem135 transgenic mice significantly overlap with those of aged mice in addition to the similarity in cardiac phenotypes, suggesting that changes in mitochondrial dynamics may be involved in the development of heart abnormalities associated with aging. Our study revealed the pathological consequence of overexpression of Tmem135, and suggested downstream molecular changes that may underlie those disease pathologies.
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