ArticleCell division2021
ROMO1 is required for mitochondrial metabolism during preimplantation embryo development in pigs.
Article in Cell division, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- ROMO1: A Distinct Mitochondrial Protein with Dual Roles in Dynamics and Function.Antioxidants (Basel, Switzerland) · 2025Article
- A Multi-omics approach to identify and validate shared genetic architecture in rheumatoid arthritis, multiple sclerosis, and type 1 diabetes: integrating GWAS, GEO, MSigDB, and scRNA-seq data.Functional & integrative genomics · 2025Article
- Oxidative and Molecular-Structural Alterations of Spermatozoa in Swine and Ram Exposed to the Triazole Ipconazole.Toxics · 2025Article
- ATF6 aggravates apoptosis in early porcine embryonic development by regulating organelle homeostasis under high-temperature conditions.Zoological research · 2023Article
- Alpha-lipoic acid attenuates heat stress-induced apoptosis via upregulating the heat shock response in porcine parthenotes.Scientific reports · 2023Article
- ATF7-dependent epigenetic changes induced by high temperature during early porcine embryonic development.Cell proliferation · 2023Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundReactive oxygen species (ROS) modulator 1 (ROMO1) is a mitochondrial membrane protein that is essential for the regulation of mitochondrial ROS production and redox sensing. ROMO1 regulates ROS generation within cells and is involved in cellular processes, such as cell proliferation, senescence, and death. Our purpose is to investigates the impact of ROMO1 on the mitochondria during porcine embryogenesis.
resultsWe found that high expression of ROMO1 was associated with porcine preimplantation embryo development, indicating that ROMO1 may contribute to the progression of embryogenesis. Knockdown of ROMO1 disrupted porcine embryo development and blastocyst quality, thereby inducing ROS production and decreasing mitochondrial membrane potential. Knockdown of ROMO1 induced mitochondrial dysfunction by disrupting the balance of OPA1 isoforms to release cytochrome c, reduce ATP, and induce apoptosis. Meanwhile, ROMO1 overexpression showed similar effects as ROMO1 KD on the embryos. Overexpression of ROMO1 rescued the ROMO1 KD-induced defects in embryo development, mitochondrial fragmentation, and apoptosis.
conclusionsROMO1 plays a critical role in embryo development by regulating mitochondrial morphology, function, and apoptosis in pigs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.