Mitochondria cannot be made de novo but replicate by a mechanism of recruitment of new proteins, which are added to preexisting subcompartments. Although mitochondria have their own DNA, more than 98% of the total protein complement of the organelle is encoded by the nuclear genome. Mitochondrial biogenesis requires a coordination of expression of two genomes and therefore cross talk between the nucleus and mitochondria. In mammals, regulation of mitochondrial biogenesis and proliferation is influenced by external factors, such as nutrients, hormones, temperature, exercise, hypoxia, and aging. This complexity points to the existence of a coordinated and tightly regulated network connecting different pathways. Communications are also required for eliciting mitochondrial responses to specific stress pathways. This review covers the mechanisms of mitochondrial biogenesis and the way cells respond to external signals to maintain mitochondrial function and cellular homeostasis.
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http://dx.doi.org/10.1146/annurev.biochem.76.052305.091720 | DOI Listing |
Nutrients
January 2025
BiOSSE, Biology of Organisms, Stress, Health, Environment, Institut Universitaire de Technologie, Département Génie Biologique, Le Mans Université, 53020 Laval, France.
Background: Physical activity, such as running, protects against cardiovascular disease and obesity but can induce oxidative stress. Athletes often consume antioxidants to counteract the overproduction of reactive oxygen and nitrogen species during exercise. , particularly its phycocyanin content, activates the Nrf2 pathway, stimulating antioxidant responses.
View Article and Find Full Text PDFPharmaceuticals (Basel)
January 2025
Department of Cardiac Surgery, Michigan Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Mitochondria dysfunction plays a central role in the development of vascular diseases as oxidative stress promotes alterations in mitochondrial morphology and function that contribute to disease progression. Redox imbalances can affect normal cellular processes including mitochondrial biogenesis, electrochemical equilibrium, and the regulation of mitochondrial DNA. In this review, we will discuss these imbalances and, in particular, the potential role of mitochondrial fusion, fission, biogenesis, and mitophagy in the context of vascular diseases and how the dysregulation of normal function might contribute to disease progression.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
College of Pharmacy, California Northstate University, Elk Grove, CA 95757, USA.
Over-accumulation of reactive oxygen species (ROS) causes hepatocyte dysfunction and apoptosis that might lead to the progression of liver damage. Sirtuin-3 (SIRT3), the main NAD+-dependent deacetylase located in mitochondria, has a critical role in regulation of mitochondrial function and ROS production as well as in the mitochondrial antioxidant mechanism. This study explores the roles of astragaloside IV (AST-IV) and formononetin (FMR) in connection with SIRT3 for potential antioxidative effects.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
School of Medicine and Surgery, University of Milano-Bicocca, 20900 Monza, Italy.
MicroRNAs (miRNAs) are a class of small non-coding RNAs (ncRNAs) crucial for regulating gene expression at the post-transcriptional level. Recent evidence has shown that miRNAs are also found in mitochondria, organelles that produce energy in the cell. These mitochondrial miRNAs, also known as mitomiRs, are essential for regulating mitochondrial function and metabolism.
View Article and Find Full Text PDFMedicina (Kaunas)
January 2025
Department of Pathology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou 225300, China.
Mitochondria play key roles in maintaining cell life and cell function, and their dysfunction can lead to cell damage. Mitochondrial ribosomal proteins (MRPs) are encoded by nuclear genes and are assembled within the mitochondria. MRPs are pivotal components of the mitochondrial ribosomes, which are responsible for translating 13 mitochondrial DNA-encoded proteins essential for the mitochondrial respiratory chain.
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