Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2024, Номер 1870(7), С. 167349 - 167349
Опубликована: Июль 14, 2024
Язык: Английский
Cancer Cell International, Год журнала: 2025, Номер 25(1)
Опубликована: Март 7, 2025
Ferroptosis is a distinct form of regulated cell death characterized by iron-dependent lipid peroxidation, playing critical role in various diseases, including cancer, neurodegeneration, and tissue damage. This study reviews the intricate relationship between ferroptosis Janus kinase/signal transducer activator transcription (JAK/STAT) signaling pathway, highlighting its regulatory functions across multiple biological processes. Dysregulation JAK/STAT pathway implicated promoting or inhibiting ferroptosis, depending on context. JAK2 promotes activating STAT proteins, modulating expression key regulators like SLC7A11 GPX4, influencing iron homeostasis through pathways such as ferritinophagy hepcidin regulation. STAT1 activation primarily enhances suppression cystine-glutamate antiporter (System Xc-), leading to glutathione depletion contributing conditions Sjogren's syndrome age-related macular degeneration. In contrast, STAT3 plays protective upregulating which inhibits survival, particularly cancers hepatocellular carcinoma, prostate renal carcinoma. also discusses STAT6's involvement diseases asthma lung injury regulating antioxidant defenses. Furthermore, review explores potential therapeutic strategies targeting manipulate for disease treatment. cancer therapy, this can enhance effectiveness inducers, offering promising avenues overcome drug resistance. Additionally, interplay immune responses, oxidative stress, metabolism underscores significance progression intervention. By exploring these mechanisms, provides insights into development novel treatments modulation, with implications inflammatory neurodegenerative conditions.
Язык: Английский
Процитировано
1
Clinical and Translational Discovery, Год журнала: 2024, Номер 4(2)
Опубликована: Апрель 1, 2024
Abstract Amino acids are necessary for all life forms, which play various roles. Disorder of amino acid metabolism is now considered an important driving mechanism in diverse pulmonary conditions, particularly chronic lung diseases like obstructive disease, idiopathic fibrosis and cancer. Glutamate actively participates multiple vital biological processes, while the intricate glutamate metabolism, receptors transporters assume crucial regulatory functions development diseases. This review aims to discuss relationship between dysfunction By discussing physiological pathological function glutamate, we probe potential drug targets pathway.
Язык: Английский
Процитировано
3
International Immunopharmacology, Год журнала: 2024, Номер 143, С. 113539 - 113539
Опубликована: Ноя. 1, 2024
Язык: Английский
Процитировано
3
Advanced Science, Год журнала: 2025, Номер unknown
Опубликована: Март 7, 2025
Cisplatin can cause irreversible hearing loss. However, effective approaches to its prevention are not established. In this study, the effect of traditional Chinese medicine monomer pinoresinol diglucoside (PDG) is evaluated on cisplatin-induced ototoxicity and underlying mechanism action. PDG significantly increases cell viability inhibits reactive oxygen species production ferroptosis in cisplatin-treated House Ear Institute-Organ Corti 1 cells basilar membranes. partially restores loss caused by cisplatin. Transcriptome sequencing identifies Suppressor Cytokine Signaling (SOCS1), which elevated cisplatin-only group but reduced after application. SOCS1 a ferroptosis-promoting factor, knocking it down nuclear receptor coactivator 4 (NCOA4) ferritinophagy. Transmission electron microscopy reveals that reduces number autophagic lysosomes induced Co-immunoprecipitation performed confirm interaction between NCOA4. Taken together, these results indicate NCOA4-mediated ferritinophagy downregulating SOCS1, ototoxicity. This study provides new clinical option for
Язык: Английский
Процитировано
0
Phytomedicine, Год журнала: 2025, Номер 142, С. 156728 - 156728
Опубликована: Апрель 5, 2025
Язык: Английский
Процитировано
0
Cell Biology International, Год журнала: 2025, Номер unknown
Опубликована: Апрель 22, 2025
ABSTRACT Ferroptosis, a unique form of regulated cell death driven by iron accumulation and lipid peroxidation, has emerged as critical process in various diseases. Recent evidence suggests its involvement the pathogenesis allergic diseases, including asthma, rhinitis, atopic dermatitis. These conditions are characterized chronic inflammation, oxidative stress, immune dysregulation, all which intersect with molecular mechanisms ferroptosis. Key regulators, such glutathione peroxidase 4 (GPX4), cystine/glutamate antiporter system Xc‐, metabolism pathways, play pivotal roles ferroptotic processes their contribution to disease progression. This review explores mechanistic link between ferroptosis emphasizing how damage overload exacerbate inflammation tissue injury. We also highlight emerging diagnostic biomarkers, peroxidation products could improve monitoring stratification. Therapeutic strategies targeting ferroptosis, GPX4 activators, chelators, inhibitors, show promise preclinical\ studies, offering potential new avenues for treating However, challenges remain translating these findings into clinical applications. By integrating current knowledge, this underscores need further research both biomarker therapeutic target
Язык: Английский
Процитировано
0
Theranostics, Год журнала: 2024, Номер 14(18), С. 6947 - 6968
Опубликована: Окт. 21, 2024
Rationale: Ferroptosis in lung epithelium and endothelium contributes to the pathogenesis of acute respiratory distress syndrome (ARDS), a critical often fatal condition marked by inflammation elevated pulmonary vascular permeability. Despite this, there are currently no FDA-approved therapeutics specifically targeting ferroptosis for ARDS management. Methods: A screening 259 drugs was conducted identify an effective inhibitor epithelial endothelial cells. The anti-ferroptotic therapeutic efficacy this screened drug rigorously evaluated using two distinct mouse models (LPS-induced injury CLP-induced sepsis) human airway organoids (hAOs). regulatory mechanism on inhibition investigated via RNA-sequencing, qRT-PCR, western blotting, IF, luciferase reporter assay, chromatin immunoprecipitation limited proteolysis-mass spectrometry cellular thermal shift affinity responsive target stability assay. Furthermore, proof-of-concept clinical trial conducted, wherein patients were administered with as adjunctive therapy. Results: Dipyridamole (DIPY) identified potent DIPY effectively mitigated damage both hAOs, primarily downregulating heme oxygenase 1 (HMOX1). transcription factor cAMP element binding protein (CREB1) key transactivator HMOX1, which downregulated. Mechanistically, binds activates superoxide dismutase (SOD1), turn inhibits CREB1/HMOX1 pathway, thereby suppressing ferroptosis. Notably, further corroborated potential patients, demonstrating improved outcomes Conclusions: These findings provide compelling evidence that cells modulating SOD1/CREB1/HMOX1 signaling axis suggest promising strategy treatment.
Язык: Английский
Процитировано
2
Journal of Ethnopharmacology, Год журнала: 2024, Номер 338, С. 119038 - 119038
Опубликована: Ноя. 6, 2024
Язык: Английский
Процитировано
2
Respiratory Research, Год журнала: 2024, Номер 25(1)
Опубликована: Дек. 6, 2024
The TGF-β/SMAD signaling pathway is crucial in the pathogenesis of asthma. However, SMAD family member 4 (SMAD4), a key mediator TGF-β, its roles and underlying mechanisms asthma remain unclear. vivo vitro SMAD4 were investigated through an ovalbumin (OVA)-induced mouse model interleukin-13 (IL-13)-induced cell model. molecular mechanism influenced was examined using transcriptome sequencing, followed by feedback experiments involving recombinant human interleukin 17 A (rhIL-17 A), IL-17 activator. highly expressed models. silencing alleviated damage to lung tissue decreased inflammatory infiltration. Expression levels Caspase-3, IgG, factors reduced after SMAD4. Silencing suppressed ferroptosis. also enhanced IL-13-induced BEAS-2B proliferation apoptosis. Furthermore. promoted models, as evidenced elevated IL-17RA, A, Act1 protein levels. inhibited expression these pathway-associated proteins. Moreover, rhIL-17 treatment notably reversed impacts on OVA-induced model, indicating that inflammation ferroptosis blocking pathway. prevents inhibiting pathway, which provides novel potential approach for therapy.
Язык: Английский
Процитировано
2
Advanced Functional Materials, Год журнала: 2024, Номер 34(44)
Опубликована: Май 29, 2024
Abstract Current diagnostic technique in direct identification of multi‐site plaques and simultaneous assessment plaque vulnerability remains a challenge, which is crucial for indicating the risk atherosclerotic cardiovascular diseases (ASCVD). Herein, an osteopontin (OPN)‐specific nanoprobe (OPN Ab‐Au/FeNiPO 4 @ICG) with both multiple spectra optoacoustic tomography (MSOT) computed (CT) imaging, constructed successfully realizing systemic screening vulnerable plaque. OPN @ICG specifically targeted OPN‐overexpressed foam cells recognized at molecular level. In AS mice, CT imaging exhibits that effectively avoid interference from calcification accurately visualized MSOT functional results reveals after injection nanoprobe, carotid exhibited much higher signal than aortic arch ( P = 0.0291). Further pathological analysis displays possessed score 0.0247), agreement signals. More importantly, linear regression confirms high correlation between signals R 0.7095 0.0216), demonstrating potential proposed systematic evaluation vulnerability. This work employs dual‐model strategy localization assessment, greatly advancing accurate diagnosis ASCVD.
Язык: Английский
Процитировано
1