APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(11-12), P. 1914 - 1943
Published: July 15, 2024
Language: Английский
APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(11-12), P. 1914 - 1943
Published: July 15, 2024
Language: Английский
Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)
Published: July 29, 2023
Abstract Programmed cell death (PCD) plays an important role in many aspects of individual development, maintenance body homeostasis and pathological processes. Ferroptosis is a novel form PCD characterized by the accumulation iron-dependent lipid peroxides resulting lethal damage. It contributes to tumor progression apoptosis-independent manner. In recent years, increasing number non-coding RNAs (ncRNAs) have been demonstrated mediate biological process ferroptosis, hence impacting carcinogenesis, progression, drug resistance, prognosis. However, clear regulatory mechanism for this phenomenon remains poorly understood. Moreover, ferroptosis does not usually exist independently. Its interaction with PCD, like apoptosis, necroptosis, autophagy, pyroptosis, cuproptosis, destroy cells appears exist. Furthermore, ncRNA seems be involved. Here, we review mechanisms which occurs, dissect its relationship other forms death, summarize key roles played ncRNAs, raise relevant questions predict possible barriers application clinic, offering new ideas targeted tumour therapy.
Language: Английский
Citations
19Journal of Colloid and Interface Science, Journal Year: 2024, Volume and Issue: 663, P. 787 - 800
Published: March 2, 2024
Language: Английский
Citations
8Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)
Published: May 8, 2024
Abstract Development of ferroptosis-inducible nanoplatforms with high efficiency and specificity is highly needed challenging in tumor ferrotherapy. Here, we demonstrate effective ferrotherapy using iron (II)-based metal-organic framework (Fe ss MOF) nanoparticles, assembled from disulfide bonds ferrous ions. The as-prepared Fe MOF nanoparticles exhibit peroxidase-like activity pH/glutathione-dependent degradability, which enables tumor-responsive catalytic therapy glutathione depletion by the thiol/disulfide exchange to suppress peroxidase 4, respectively. Upon PEGylation Actinomycin D (ActD) loading, resulting MOF/ActD-PEG nanoplatform induces marked DNA damage lipid peroxidation. Concurrently, found that ActD can inhibit Xc − system elicit ferritinophagy, further boosts ferrotherapeutic efficacy MOF/ActD-PEG. In vivo experiments our fabricated presents excellent biocompatibility a inhibition rate 91.89%.
Language: Английский
Citations
8Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)
Published: June 24, 2024
Abstract Pulmonary fibrosis (PF) is a chronic interstitial lung disorder characterized by abnormal myofibroblast activation, accumulation of extracellular matrix (ECM), and thickening fibrotic alveolar walls, resulting in deteriorated function. PF initiated dysregulated wound healing processes triggered factors such as excessive inflammation, oxidative stress, coronavirus disease (COVID-19). Despite advancements understanding the disease’s pathogenesis, effective preventive therapeutic interventions are currently lacking. Ferroptosis, an iron-dependent regulated cell death (RCD) mechanism involving lipid peroxidation glutathione (GSH) depletion, exhibits unique features distinct from other RCD forms (e.g., apoptosis, necrosis, pyroptosis). Imbalance between reactive oxygen species (ROS) production detoxification leads to ferroptosis, causing cellular dysfunction through peroxidation, protein modifications, DNA damage. Emerging evidence points crucial role ferroptosis progression, driving macrophage polarization, fibroblast proliferation, ECM deposition, ultimately contributing tissue scarring. This review provides comprehensive overview latest findings on involvement signaling mechanisms emphasizing potential novel anti-fibrotic approaches targeting for management.
Language: Английский
Citations
8APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(11-12), P. 1914 - 1943
Published: July 15, 2024
Language: Английский
Citations
7