PM2.5 Induces Developmental Neurotoxicity in Cortical Organoids

Environmental Pollution, Journal Year: 2024, Volume and Issue: 361, P. 124913 - 124913

Published: Sept. 6, 2024

Language: Английский

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Integrative analysis of genes provides insights into the molecular and immune characteristics of mitochondria-related genes in atherosclerosis

Genomics, Journal Year: 2025, Volume and Issue: 117(2), P. 111013 - 111013

Published: Feb. 4, 2025

Language: Английский

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Ferroptosis and hyperoxic lung injury: insights into pathophysiology and treatment approaches

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 18, 2025

Hyperoxia therapy is a critical clinical intervention for both acute and chronic illnesses. However, prolonged exposure to high-concentration oxygen can cause lung injury. The mechanisms of hyperoxic injury (HLI) remain incompletely understood, current treatment options are limited. Improving the safety hyperoxia has thus become an urgent priority. Ferroptosis, novel form regulated cell death characterized by iron accumulation excessive lipid peroxidation, been implicated in pathogenesis HLI, including diffuse alveolar damage, vascular endothelial injury, bronchopulmonary dysplasia. In this review, we analyze latest findings on ferroptosis therapeutic strategies HLI. Our aim provide new insights HLI facilitate translation these from bench bedside.

Language: Английский

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Cell life-or-death events in osteoporosis: All roads lead to mitochondrial dynamics

Pharmacological Research, Journal Year: 2024, Volume and Issue: 208, P. 107383 - 107383

Published: Aug. 28, 2024

Mitochondria exhibit heterogeneous shapes and networks within among cell types tissues, also in normal or osteoporotic bone tissues with complex types. This dynamic characteristic is determined by the high plasticity provided mitochondrial dynamics stemmed from responding to survival functional requirements of various cells a specific microenvironments. In contrast, dysfunction, induced dysregulation dynamics, may act as trigger death signals, including common apoptosis other forms programmed (PCD). These PCD processes consisting tightly structured cascade gene expression events, can further influence remodeling facilitating cells. Mitochondrial therefore, drive stand at crossroads life integrating external signals altering metabolism, shape, signal-response properties mitochondria. implies that targeting displays significant potential treatment osteoporosis. Considerable effort has been made osteoporosis emphasize parallel roles mitochondria regulating energy calcium signal transduction, oxidative stress, inflammation, death. However, emerging field dynamics-related not well understood. Herein, bridge gap, we outline latest knowledge on during

Language: Английский

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Marsdenia tenacissima extract accelerates ferroptosis of osteosarcoma cells by upregulating HO-1 and activating mitophagy

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 120055 - 120055

Published: May 1, 2025

Language: Английский

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Mitophagy-associated programmed neuronal death and neuroinflammation

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 2, 2024

Mitochondria are crucial organelles that play a central role in cellular metabolism and programmed cell death eukaryotic cells. Mitochondrial autophagy (mitophagy) is selective process where damaged mitochondria encapsulated degraded through autophagic mechanisms, ensuring the maintenance of both mitochondrial homeostasis. Excessive neurons can result functional impairments following cerebral ischemia trauma, as well chronic neurodegenerative diseases, leading to irreversible declines motor cognitive functions. Neuroinflammation, an inflammatory response nervous system factors disrupting homeostasis, common feature across various neurological events, including ischemic, infectious, traumatic, conditions. Emerging research suggests regulating may offer promising therapeutic avenue for treating certain diseases. Furthermore, existing literature indicates small molecule regulators have been tested animal models linked disease outcomes. This review explores mitophagy neuronal its connection neuroinflammation.

Language: Английский

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Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures

Environment International, Journal Year: 2024, Volume and Issue: 195, P. 109193 - 109193

Published: Dec. 13, 2024

Fine particulate matter (PM2.5) is increasingly recognized for its detrimental effects on human health, with substantial evidence linking exposure to various forms of cell death and dysfunction across multiple organ systems. This review examines key mechanisms triggered by PM2.5, including PANoptosis, necroptosis, autophagy, ferroptosis, while other such as oncosis, paraptosis, cuprotosis remain unreported in relation PM2.5 exposure. Mitochondria, endoplasmic reticulum, lysosomes emerge pivotal organelles the disruption cellular homeostasis, mitochondrial particularly implicated metabolic dysregulation activation pro-apoptotic pathways. Although primarily affects nucleus, cytoskeleton, mitochondria, lysosomes, like ribosomes, Golgi apparatus, peroxisomes have received limited attention. Interactions between these organelles, reticulum-associated membranes, lysosome-associated mitophagy, mitochondria-nuclei retro-signaling may significantly contribute cytotoxic PM2.5. The toxicity, encompassing oxidative stress, inflammatory responses, imbalances, are described detail. Notably, activates NLRP3 inflammasome, amplifying responses contributing chronic diseases. Furthermore, disrupts genetic epigenetic regulation, often resulting cycle arrest exacerbating damage. composition, concentration, seasonal variability modulate effects, underscoring complexity PM2.5-induced dysfunction. Despite significant advances understanding pathways, further research required elucidate long-term exposure, role potential strategies mitigate harmful impact health.

Language: Английский

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Relationship between ferroptosis and mitophagy in acute lung injury: a mini-review

PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e18062 - e18062

Published: Sept. 10, 2024

Acute lung injury (ALI) is one of the most deadly and prevalent diseases in intensive care unit. Ferroptosis mitophagy are pathological mechanisms ALI. aggravates ALI, whereas regulates both closely related to reactive oxygen species (ROS). Mitophagy can regulate ferroptosis, but specific relationship between ferroptosis still unclear. This study summarizes previous research findings on mitophagy, revealing their involvement Examining functions mTOR NLPR3 helps clarify connection with goal establishing a theoretical foundation for potential therapeutic approaches future management

Language: Английский

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Fighting ferroptosis: Protective effects of dexmedetomidine on vital organ injuries

Life Sciences, Journal Year: 2024, Volume and Issue: 354, P. 122949 - 122949

Published: Aug. 8, 2024

Language: Английский

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Serum pharmacochemistry combined with network pharmacology reveals the hepatotoxicity mechanism of Alangium chinense (Lour.) Harms

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 340, P. 119312 - 119312

Published: Dec. 31, 2024

Language: Английский

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