Neuropharmacology, Год журнала: 2025, Номер unknown, С. 110439 - 110439
Опубликована: Март 1, 2025
Язык: Английский
Cell, Год журнала: 2024, Номер 187(11), С. 2601 - 2627
Опубликована: Май 1, 2024
Mitochondria reside at the crossroads of catabolic and anabolic metabolism—the essence life. How their structure function are dynamically tuned in response to tissue-specific needs for energy, growth repair, renewal is being increasingly understood. respond intrinsic extrinsic stresses can alter cell organismal by inducing metabolic signaling within cells distal tissues. Here, we review how centrality mitochondrial functions manifests health a broad spectrum diseases aging.
Язык: Английский
Процитировано
105
Nature Cancer, Год журнала: 2024, Номер 5(3), С. 384 - 399
Опубликована: Март 22, 2024
Язык: Английский
Процитировано
61
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(2), С. 1314 - 1314
Опубликована: Янв. 21, 2024
Mitochondria are critical for providing energy to maintain cell viability. Oxidative phosphorylation involves the transfer of electrons from substrates oxygen produce adenosine triphosphate. also regulate proliferation, metastasis, and deterioration. The flow in mitochondrial respiratory chain generates reactive species (ROS), which harmful cells at high levels. stress caused by ROS accumulation has been associated with an increased risk cancer, cardiovascular liver diseases. Glutathione (GSH) is abundant cellular antioxidant that primarily synthesized cytoplasm delivered mitochondria. Mitochondrial glutathione (mGSH) metabolizes hydrogen peroxide within A long-term imbalance ratio mGSH can cause dysfunction, apoptosis, necroptosis, ferroptosis, may lead disease. This study aimed review physiological functions, anabolism, variations organ tissue accumulation, delivery GSH mitochondria relationships between levels, GSH/GSH disulfide (GSSG) ratio, programmed death, ferroptosis. We discuss diseases deficiency related therapeutics.
Язык: Английский
Процитировано
54
Trends in Endocrinology and Metabolism, Год журнала: 2024, Номер unknown
Опубликована: Май 1, 2024
Iron deficiency is globally prevalent, causing an array of developmental, haematological, immunological, neurological, and cardiometabolic impairments, associated with symptoms ranging from chronic fatigue to hair loss. Within cells, iron utilised in a variety ways by hundreds different proteins. Here, we review links between molecular activities regulated the pathophysiological effects deficiency. We identify specific enzyme groups, biochemical pathways, cellular functions, cell lineages that are particularly dependent. provide examples how deprivation influences multiple key systems tissues, including immunity, hormone synthesis, cholesterol metabolism. propose greater mechanistic understanding physiological processes may lead new therapeutic opportunities across range diseases.
Язык: Английский
Процитировано
16
Trends in Endocrinology and Metabolism, Год журнала: 2024, Номер 35(5), С. 385 - 399
Опубликована: Янв. 22, 2024
Язык: Английский
Процитировано
11
EBioMedicine, Год журнала: 2025, Номер 112, С. 105533 - 105533
Опубликована: Янв. 13, 2025
Язык: Английский
Процитировано
1
Cell, Год журнала: 2025, Номер 188(4), С. 869 - 884
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
1
Molecular Cell, Год журнала: 2023, Номер 84(4), С. 802 - 810.e6
Опубликована: Дек. 28, 2023
Язык: Английский
Процитировано
20
Nature Communications, Год журнала: 2024, Номер 15(1)
Опубликована: Май 18, 2024
Abstract Cysteine metabolism occurs across cellular compartments to support diverse biological functions and prevent the induction of ferroptosis. Though disruption cytosolic cysteine is implicated in this form cell death, it unknown whether substantial resident within mitochondria similarly pertinent Here, we show that despite rapid depletion intracellular upon loss extracellular cystine, cysteine-dependent synthesis Fe-S clusters persists lung cancer cells. This promotes a retention respiratory function maintenance mitochondrial redox state. Under these limiting conditions, find glutathione catabolism by CHAC1 supports pool sustain proteins critical oxidative metabolism. We disrupting cluster under restriction protects against ferroptosis, suggesting preservation antagonistic survival starved conditions. Overall, our findings implicate ferroptosis reveal mechanism resilience response nutrient stress.
Язык: Английский
Процитировано
8
Molecular Biomedicine, Год журнала: 2024, Номер 5(1)
Опубликована: Ноя. 29, 2024
Abstract Tumor energy metabolism plays a crucial role in the occurrence, progression, and drug resistance of tumors. The study tumor has gradually become an emerging field treatment. Recent studies have shown that epigenetic regulation is closely linked to metabolism, influencing metabolic remodeling biological traits cells. This review focuses on primary pathways explores therapeutic strategies target these pathways. It covers key areas such as glycolysis, Warburg effect, mitochondrial function, oxidative phosphorylation, adaptability Additionally, this article examines regulator SWI/SNF complex specifically its interactions with glucose, lipids, amino acids. Summarizing aimed at pathways, including inhibitors mitochondrial-targeted drugs, exploitation vulnerabilities, recent developments related complexes potential targets. clinical significance, challenges, future directions research are discussed, overcome resistance, combination therapy, application new technologies.
Язык: Английский
Процитировано
8