Mitochondria are known as the powerhouses of eukaryotic cells; however, they perform many other functions besides oxidative phosphorylation, including Ca homeostasis, lipid metabolism, antiviral response, and apoptosis. Although other hypotheses exist, mitochondria are generally thought as descendants of an α-proteobacteria that adapted to the intracellular environment within an Asgard archaebacteria, which have been studied for decades as an organelle subdued by the eukaryotic cell. Nevertheless, several early electron microscopy observations hinted that some mitochondria establish specific interactions with certain plasma membrane (PM) domains in mammalian cells. Furthermore, recent findings have documented the direct physical and functional interaction of mitochondria and the PM, the organization of distinct complexes, and their communication through vesicular means. In yeast, some molecular players mediating this interaction have been elucidated, but only a few works have studied this interaction in mammalian cells. In addition, mitochondria can be translocated among cells through tunneling nanotubes or by other mechanisms, and free, intact, functional mitochondria have been reported in the blood plasma. Together, these findings challenge the conception of mitochondria as organelles subdued by the eukaryotic cell. This review discusses the evidence of the mitochondria interaction with the PM that has been long disregarded despite its importance in cell function, pathogenesis, and evolution. It also proposes a scheme of mitochondria-PM interactions with the intent to promote research and knowledge of this emerging pathway that promises to shift the current paradigms of cell biology.
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http://dx.doi.org/10.1016/j.jbc.2021.101164 | DOI Listing |
Mol Cell Biochem
January 2025
Department of Clinical Biochemistry and Laboratory Diagnostics, Institute of Medical Sciences, University of Opole, Oleska 48, 45-052, Opole, Poland.
Scientific reports from various areas of the world indicate the potential role of tocopherols (vitamin E) in particular α-tocopherol in the prevention and therapy of Alzheimer's disease. The current phenomenon is related to the growing global awareness of eating habits and is also determined by the need to develop the prevention, management and therapy of Alzheimer's disease. This article is a review of current research on the action of the active form of vitamin E-α-tocopherol and its impact on the development and course of Alzheimer's disease.
View Article and Find Full Text PDFHum Cell
January 2025
The First Branch, Hongqi Hospital Affiliated to Mudanjiang Medical University, No. 5 Tongxiang Street, Aimin District, Mudanjiang, 157000, China.
Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke, and the neuroprotective effects of nimodipine following SAH have been well-documented. Sirtuin 3 (SIRT3), a mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, plays a significant role in mitigating oxidative stress in various neurodegenerative conditions. However, the role of SIRT3 in the neuroprotective mechanisms of nimodipine after SAH remains unclear.
View Article and Find Full Text PDFAdv Healthc Mater
January 2025
Department of Cardiology, Laboratory of Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, P. R. China.
Redox imbalance, including excessive production of reactive oxygen species (ROS) caused by mitochondrial dysfunction and insufficient endogenous antioxidant capacity, is the primary cause of myocardial ischemia‒reperfusion (I/R) injury. In the exploration of reducing myocardial I/R injury, it is found that protecting myocardial mitochondrial function after reperfusion not only reduces ROS bursts but also inhibits cell apoptosis triggered by the release of cytochrome c. Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) is considered a potential therapeutic target for treating myocardial I/R injury by enhancing the cellular antioxidant capacity through the induction of endogenous antioxidant enzymes.
View Article and Find Full Text PDFNanoscale
January 2025
School of Chemistry and Chemical Engineering, Center of Free Electron Laser & High Magnetic Field, Key Laboratory of Structure and Functional Regulation of Hybrid Materials Ministry of Education, Key Laboratory of Functional Inorganic Materials Chemistry of Anhui Province, and Key Laboratory of Chemistry for Inorganic/Organic Hybrid Functionalized Materials of Anhui Province, Anhui University, P.R. China.
Currently, the study of cuproptosis focuses on the Cu-induced morphology changes in mitochondria (Mito), and the observation of the effect of endoplasmic reticulum (ER)-related Cu content on cuproptosis is relatively lacking. Herein, we have developed a hydroxyflavone (HF)-based NIR excited two-photon fluorescent probe, BHCO, that exhibits specific recognition of Cu with high resolution. BHCO-Cu (Cu2BC) can lead to DLAT protein aggregation, triggering cuproptosis.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.
Chronic obstructive pulmonary disease (COPD) is a prevalent chronic respiratory disease worldwide. Mitochondrial quality control mechanisms encompass processes such as mitochondrial biogenesis, fusion, fission, and autophagy, which collectively maintain the quantity, morphology, and function of mitochondria, ensuring cellular energy supply and the progression of normal physiological activities. However, in COPD, due to the persistent stimulation of harmful factors such as smoking and air pollution, mitochondrial quality control mechanisms often become deregulated, leading to mitochondrial dysfunction.
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