Published: Jan. 1, 2024
Language: Английский
Published: Jan. 1, 2024
Language: Английский
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
Citations
14Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156658 - 156658
Published: March 1, 2025
Language: Английский
Citations
1Frontiers in Nutrition, Journal Year: 2024, Volume and Issue: 11
Published: Feb. 27, 2024
NAD + , a pivotal coenzyme central to metabolism, exhibits characteristic decline with age. In mice, levels can be elevated via treatment apigenin, natural flavonoid that inhibits the -consuming glycoprotein CD38. animal models, apigenin positively impacts both sleep and longevity. For example, improves learning memory in older reduces tumor proliferation mouse xenograft model of triple-negative breast cancer, induces sedative effects mice rats. Moreover, elongates survival fly models neurodegenerative disease glycosides increase lifespan worms. Apigenin’s therapeutic potential is underscored by human clinical studies using chamomile extract, which contains as an active ingredient. Collectively, extract has been reported alleviate anxiety, improve mood, relieve pain. Furthermore, dietary intake correlates quality large cohort adults. electron-rich structure gives it strong bonding capacity diverse molecular structures across receptors enzymes. The extend beyond CD38 inhibition, encompassing agonistic antagonistic modulation various targets, including GABA inflammatory pathways. Cumulatively, body evidence positions unique molecule capable influencing aging sleep. Further are warranted better understand apigenin’s nuanced mechanisms potential.
Language: Английский
Citations
5Discover Plants., Journal Year: 2025, Volume and Issue: 2(1)
Published: Jan. 20, 2025
Language: Английский
Citations
0The Journal of Cardiovascular Aging, Journal Year: 2025, Volume and Issue: 5(1)
Published: Jan. 22, 2025
With the increase in life expectancy globally, challenge of dealing with aging becomes more prominent. Aging is a risk factor for several diseases, including cardiovascular disease. Mitochondria, which have long been studied relation to aging, play crucial role maintaining cellular homeostasis. However, there limitation interorganellar communication as organisms age. The unfolded protein response mitochondria (UPRmt) activated during stress maintain mitochondrial homeostasis and prevent accumulation damaged mitochondria. This involves signaling from nucleus, leading transcriptional changes. In context heart, this review explores terms function morphology. It also discusses impact UPRmt on cardiac diseases such heart failure, acute myocardial infarction, dilated cardiomyopathy. highlights potential mitochondria-endoplasmic reticulum contact sites (MERCs) modulating aging. Finally, it provides an update molecules that induce activity, potentially benefiting
Language: Английский
Citations
0International Journal of Medical Sciences, Journal Year: 2025, Volume and Issue: 22(7), P. 1640 - 1657
Published: Feb. 28, 2025
Doxorubicin-induced myocardial injury, characterized by hypertrophy and heart failure (HF), represents a primary contributor to end-stage cardiovascular mortality associated with anthracycline drugs. Prior research has elucidated that SIRT6-mediated oxidative processes mitochondrial metabolic reprogramming are pivotal in sustaining energy metabolism during damage cardiomyocytes. In the aftermath of doxorubicin-induced fibrosis exacerbate impairment cardiac ejection function, resulting elevated oxygen consumption. This condition is accompanied disrupted ATP production, diminished biogenesis, inadequate synthesis new DNA, collectively triggering necroptosis apoptosis pathways. Our preliminary experimental results have confirmed SIRT6, traditional medicine, exerts cardioprotective effects. Nevertheless, interaction between SIRT6 Nrf-2-mediated biogenesis context HF remains inadequately understood. The generation mitochondria key mechanism involved DNA repair cell cycle management.
Language: Английский
Citations
0Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 330, P. 118152 - 118152
Published: April 12, 2024
Language: Английский
Citations
3Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 177, P. 116989 - 116989
Published: July 2, 2024
The mitochondrial unfolded protein response (UPRmt) is a cytoprotective in to cellular stress that activated maintain intra-protein homeostasis, thereby protecting the cell from variety of stimuli. activation this has been linked cardiovascular diseases. Here, we reviewed current understanding UPRmt and discussed its specific molecular mechanism, mainly mammals, as well addressing protective role against diseases, so provide direction for further research on therapies targeting diseases future.
Language: Английский
Citations
2Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0
Published: Jan. 1, 2024
Throughout the course of evolution, organisms and cells have evolved a suite mechanisms to manage persistent stimuli, thereby preserving cellular organismal homeostasis. Upon detecting stress signals, activate transcriptional response termed mitochondrial unfolded protein (UPRmt). This is crucial for maintaining homeostasis, facilitating function recovery, promoting cell survival, ultimately influencing lifespan. Striated muscles play pivotal role in oxygen supply, movement, metabolism. The aging these can lead heart failure, arrhythmias, sarcopenia, significantly impacting quality life Given intimate connection between UPRmt striated muscle aging, emerges as potential therapeutic target mitigating effects aging. In this review, we delve into drawing upon extant molecular regulatory UPRmt. exploration may enhance our understanding underlying aid identification drug targets.
Language: Английский
Citations
1Published: Jan. 1, 2024
Language: Английский
Citations
0