Plant Secondary Metabolites as Modulators of Mitochondrial Health: An Overview of Their Anti-Oxidant, Anti-Apoptotic, and Mitophagic Mechanisms

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(1), P. 380 - 380

Published: Jan. 4, 2025

Plant secondary metabolites (PSMs) are a diverse group of bioactive compounds, including flavonoids, polyphenols, saponins, and terpenoids, which have been recognised for their critical role in modulating cellular functions. This review provides comprehensive analysis the effects PSMs on mitochondrial health, with particular emphasis therapeutic potential. Emerging evidence shows that these improve function by reducing oxidative stress, promoting biogenesis, regulating key processes such as apoptosis mitophagy. Mitochondrial dysfunction, hallmark many pathologies, neurodegenerative disorders, cardiovascular diseases, metabolic syndrome, has shown to benefit from protective PSMs. Recent studies show can dynamics, stabilise membranes, enhance bioenergetics, offering significant promise prevention treatment mitochondrial-related diseases. The molecular mechanisms underlying effects, modulation signalling pathways direct interactions proteins, discussed. integration into strategies is highlighted promising avenue improving efficacy while minimising side commonly associated synthetic drugs. also highlights need future research elucidate specific roles individual synergistic within complex plant matrices, may further optimise utility. Overall, this work valuable insights health potential natural agents targeting dysfunction.

Language: Английский

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Exploring the Mechanism of Ferroptosis Induction by Sappanone A in Cancer: Insights into the Mitochondrial Dysfunction Mediated by NRF2/xCT/GPX4 Axis

International Journal of Biological Sciences, Journal Year: 2024, Volume and Issue: 20(13), P. 5145 - 5161

Published: Jan. 1, 2024

Non-small cell lung cancer (NSCLC), a major subtype of cancer, encompasses squamous carcinoma, adenocarcinoma, and large carcinoma. Compared to small NSCLC cells grow divide more slowly, their metastasis occurs at later stage. Currently, chemotherapy is the primary treatment for this disease. Sappanone A (SA) flavonoid compound extracted from plant Caesalpinia sappan, known its antitumor, redox-regulating, anti-inflammatory properties. Recent studies have investigated interaction SA with mitochondrial pathways in regulating death through Nrf-2/GPX-4/xCT axis. This study specifically explores mechanism by which affects morphology structure regulation mitophagy biogenesis tumor cells. The primarily utilizes second-generation transcriptomic sequencing data molecular docking techniques elucidate role programmed omics results indicate that significantly targets genes involved oxidative phosphorylation, mitophagy, dynamics, stress. Further findings confirmed Nrf-2/GPX4/xCT pathway serves as crucial target NSCLC. Knockdown Nrf-2 (si-Nrf-2) overexpression (ad-Nrf-2) were shown modulate therapeutic efficacy varying degrees. Additionally, modifications GPX4/xCT affected regulatory effects on autophagy, biogenesis, energy metabolism. These mechanisms may be mediated caspase ferroptosis-related signaling. Molecular biology experiments demonstrated intervention further inhibits phosphorylation FUNDC1 Tyr18 downregulates TOM20 expression. was found reduce expression PGC1α, Nrf-1, Tfam, resulting decrease respiration Overexpression counteract biogenesis. Confocal microscopy revealed increases fragmentation, subsequently inducing pathway-mediated death. However, genetic modification altered In conclusion, has been identified promising agent apoptosis ferroptosis represent key Targeting axis offers novel approach maintaining homeostasis within cellular microenvironment.

Language: Английский

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Enhancing fat graft survival: thymosin beta-4 facilitates mitochondrial transfer from ADSCs via tunneling nanotubes by upregulating the Rac/F-actin pathway

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: 228, P. 281 - 298

Published: Jan. 5, 2025

Language: Английский

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Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging

Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 372 - 372

Published: March 21, 2025

Mitochondria are of great importance in cell biology since they major sites adenosine triphosphate (ATP) production and widely involved different cellular pathways the response to stress. During ATP production, reactive oxygen species (ROS) can be produced. While a small amount ROS may important for regulation physiological processes, at elevated levels turn into harmful agents leading damage. From pathological perspective, it could particularly interesting focus on mitochondrial function endothelial cells development aging onset diseases, including renal, cardio-metabolic, liver neurodegenerative ones. However, date, there no surveys which address above issues. To fill this gap, valuable collect recent findings about role mitochondria function, not only increase knowledge but also clinical applications. Here, we overview most issues view characterizing as an innovative potential target prevention aging, well treatment conditions.

Language: Английский

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Neutrophil extracellular traps aggravate placental injury in OAPS by facilitating activation of BNIP3 mediated mitophagy

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: 235, P. 109 - 123

Published: April 25, 2025

Language: Английский

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Mesenchymal stromal cells deliver H2S-enhanced Nrf2 via extracellular vesicles to mediate mitochondrial homeostasis for repairing hypoxia-ischemia brain damage

Free Radical Biology and Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 1, 2024

Language: Английский

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Lysosome-Mitochondrial Crosstalk in Cellular Stress and Disease

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 125 - 125

Published: Jan. 22, 2025

The perception of lysosomes and mitochondria as entirely separate independent entities that degrade material produce ATP, respectively, has been challenged in recent years not only more complex roles for both organelles, but also an unanticipated level interdependence are being uncovered. Coupled lysosome mitochondrial function dysfunction involve crosstalk between the two organelles which goes beyond quality control lysosome-mediated clearance damaged through mitophagy. Our understanding these essential metabolic transformed by major advances field membrane contact sites biology. We now know play central inter-organelle communication. This importance mitochondria–lysosome contacts (MLCs) cellular homeostasis, evinced growing number diseases have associated with their dysregulation, is starting to be appreciated. How MLCs regulated how coordination other pathways lysosome–mitochondria achieved subjects ongoing scrutiny, this review explores current governing its impact on stress disease.

Language: Английский

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A rhodamine-coordinated iridium complex to overcome cisplatin-resistant cancer via regulating mitochondrial function triggered apoptosis and ferroptosis

Redox Biology, Journal Year: 2025, Volume and Issue: 81, P. 103536 - 103536

Published: Feb. 10, 2025

Language: Английский

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Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: March 31, 2025

Abstract Neurodegenerative disorders present significant challenges to modern medicine because of their complex etiology, pathogenesis, and progressive nature, which complicate practical treatment approaches. Mitochondrial dysfunction is an important contributor the pathophysiology various neurodegenerative illnesses, including Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS). This review paper examines current literature highlighting multifaceted functions mitochondria, energy production, calcium signaling, apoptosis regulation, mitochondrial biogenesis, dynamics, axonal transport, endoplasmic reticulum–mitochondrial interactions, mitophagy, proteostasis, crucial involvement in neuronal health. The emphasizes increasing recognition as a critical factor progression disorders, marking shift from traditional symptom management innovative mitochondrial-based therapies. By discussing mechanisms, quality control (MQC) processes impact oxidative stress, this highlights need for novel therapeutic strategies restore function, protect connections integrity, slow progression. comprehensive aims provide insights into potential interventions that could transform landscape diseases, addressing symptoms underlying pathophysiological changes.

Language: Английский

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Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation

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

Published: April 28, 2025

Mitochondria, as the primary energy factories of cells, play a pivotal role in maintaining nervous system function and regulating inflammatory responses. The balance mitochondrial quality control is critical for neuronal health, disruptions this are often implicated pathogenesis various neurological disorders. Mitochondrial dysfunction not only exacerbates deficits but also triggers neuroinflammation through release damage-associated molecular patterns (DAMPs), such DNA (mtDNA) reactive oxygen species (ROS). This review examines mechanisms recent advancements diseases, focusing on processes fusion fission, mitophagy, biogenesis, protein expression regulation. It further explores subsequent cascades conditions ischemic hemorrhagic stroke, neurodegenerative diseases brain tumors. Additionally, emerging research highlights significance transfer mechanisms, particularly intercellular between neurons glial potential strategy mitigating inflammation promoting cellular repair. provides insights into underpinnings neuroinflammatory pathologies while underscoring translational targeting therapeutic development.

Language: Английский

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