Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)
Published: Aug. 27, 2024
Abstract The development of drug resistance remains a major challenge in cancer treatment. Ferroptosis, unique type regulated cell death, plays pivotal role inhibiting tumour growth, presenting new opportunities treating chemotherapeutic resistance. Accumulating studies indicate that epigenetic modifications by non-coding RNAs (ncRNA) can determine vulnerability to ferroptosis. In this review, we first summarize the growth/development. Then, core molecular mechanisms ferroptosis, its upstream regulation, and downstream effects on Finally, review recent advances understanding how ncRNAs regulate ferroptosis from such modulate This aims enhance general ncRNA-mediated regulatory which highlighting ncRNA-ferroptosis axis as key druggable target overcoming
Language: Английский
Citations
14
Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)
Published: Sept. 28, 2024
Language: Английский
Citations
14
Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(8)
Published: April 9, 2024
Abstract Chemotherapy, radiotherapy, and immunotherapy represent key tumour treatment strategies. Notably, immune checkpoint inhibitors (ICIs), particularly anti‐programmed cell death 1 (PD1) ligand (PD‐L1), have shown clinical efficacy in immunotherapy. However, the limited effectiveness of ICIs is evident due to many cancers exhibiting poor responses this treatment. An emerging avenue involves triggering non‐apoptotic regulated (RCD), a significant mechanism driving cancer diverse treatments. Recent research demonstrates that combining RCD inducers with significantly enhances their antitumor across various types. The use anti‐PD‐1/PD‐L1 activates CD8 + T cells, prompting initiation novel forms, such as ferroptosis, pyroptosis, necroptosis. functions mechanisms anti‐PD1/PD‐L1 therapy remain insufficiently explored. This review summarises roles necroptosis It emphasises synergy between nanomaterials PD‐1/PD‐L1 induce different Furthermore, targeting signalling pathways combination therapies holds promise prospective strategy for
Language: Английский
Citations
13
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(7), P. 4087 - 4087
Published: April 6, 2024
Cellular survival hinges on a delicate balance between accumulating damages and repair mechanisms. In this intricate equilibrium, oxidants, currently considered physiological molecules, can compromise vital cellular components, ultimately triggering cell death. On the other hand, cells possess countermeasures, such as autophagy, which degrades recycles damaged molecules organelles, restoring homeostasis. Lysosomes their enzymatic arsenal, including cathepsins, play critical roles in balance, influencing cell’s fate toward either apoptosis mechanisms of regulated death or autophagy. However, interplay reactive oxygen species (ROS) cathepsins these life-or-death pathways transcends simple cause-and-effect relationship. These elements directly indirectly influence each other’s activities, creating complex web interactions. This review delves into inner workings highlighting pivotal role ROS interplay.
Language: Английский
Citations
12
Trends in Endocrinology and Metabolism, Journal Year: 2024, Volume and Issue: unknown
Published: May 1, 2024
Iron deficiency is globally prevalent, causing an array of developmental, haematological, immunological, neurological, and cardiometabolic impairments, associated with symptoms ranging from chronic fatigue to hair loss. Within cells, iron utilised in a variety ways by hundreds different proteins. Here, we review links between molecular activities regulated the pathophysiological effects deficiency. We identify specific enzyme groups, biochemical pathways, cellular functions, cell lineages that are particularly dependent. provide examples how deprivation influences multiple key systems tissues, including immunity, hormone synthesis, cholesterol metabolism. propose greater mechanistic understanding physiological processes may lead new therapeutic opportunities across range diseases.
Language: Английский
Citations
12
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(14), P. 7544 - 7544
Published: July 9, 2024
Ferroptosis is a type of nonapoptotic cell death that characteristically caused by phospholipid peroxidation promoted radical reactions involving iron. Researchers have identified many the protein factors are encoded genes promote ferroptosis. Glutathione peroxidase 4 (GPX4) key enzyme protects phospholipids from and suppresses ferroptosis in glutathione-dependent manner. Thus, dysregulation involved cysteine and/or glutathione metabolism closely associated with From perspective dynamics, actively proliferating cells more prone to than quiescent cells, which suggests species generated during oxygen-involved responsible for lipid peroxidation. Herein, we discuss initial events dominantly occur process energy metabolism, association deficiency. Accordingly, tricarboxylic acid cycle coupled respiratory chain mitochondria main subjects here, this likely source both electrons free Since not only carbohydrates, but also amino acids, especially glutamate, major substrates central dealing nitrogen derived groups contributes subject discussion.
Language: Английский
Citations
12
MedComm, Journal Year: 2024, Volume and Issue: 5(9)
Published: Sept. 1, 2024
Abstract Cell death regulation is essential for tissue homeostasis and its dysregulation often underlies cancer development. Understanding the different pathways of cell can provide novel therapeutic strategies battling cancer. This review explores several key mechanisms apoptosis, necroptosis, autophagic death, ferroptosis, pyroptosis. The research gap addressed involves a thorough analysis how these be precisely targeted therapy, considering tumor heterogeneity adaptation. It delves into genetic epigenetic factors signaling cascades like phosphatidylinositol 3‐kinase/protein kinase B/mammalian target rapamycin (PI3K/AKT/mTOR) mitogen‐activated protein kinase/extracellular signal‐regulated (MAPK/ERK) pathways, which are critical death. Additionally, interaction microenvironment with cells, particularly influence hypoxia, nutrient deprivation, immune cellular interactions, explored. Emphasizing strategies, this highlights emerging modulators inducers such as B lymphoma 2 (BCL2) homology domain 3 (BH3) mimetics, tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL), chloroquine, innovative approaches to induce ferroptosis provides insights therapy's future direction, focusing on multifaceted circumvent drug resistance. examination evolving underlines considerable clinical potential continuous necessity in‐depth exploration within scientific domain.
Language: Английский
Citations
12
Seminars in Cancer Biology, Journal Year: 2024, Volume and Issue: 106-107, P. 156 - 165
Published: Oct. 16, 2024
Language: Английский
Citations
10
Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: July 3, 2024
Ferroptosis is a form of non-apoptotic regulated cell death (RCD) that depends on iron and characterized by the accumulation lipid peroxides to lethal levels. involves multiple pathways including redox balance, regulation, mitochondrial function, amino acid, lipid, glycometabolism. Furthermore, various disease-related signaling also play role in regulating process oxidation. In recent years, with emergence concept ferroptosis in-depth study its mechanisms, closely associated biological conditions related kidney diseases, organ development, aging, immunity, cancer. This article reviews development ferroptosis, mechanisms (including GSH-GPX4, FSP1-CoQ1, DHODH-CoQ10, GCH1-BH4, MBOAT1/2 pathways), latest research progress involvement diseases. It summarizes diseases within frameworks metabolism, reactive oxygen biology, biology. The introduces key regulatory factors as well important concepts major open questions natural compounds. hoped future research, further breakthroughs can be made understanding regulation mechanism utilizing promote treatments for such acute injury(AKI), chronic disease (CKD), diabetic nephropathy(DN), renal carcinoma. paves way new approach prevent, treat clinical
Language: Английский
Citations
9
Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(7)
Published: July 4, 2024
Abstract Autoimmune diseases commonly affect various systems, but their etiology and pathogenesis remain unclear. Currently, increasing research has highlighted the role of ferroptosis in immune regulation, with cells being a crucial component body’s system. This review provides an overview discusses relationship between ferroptosis, programmed cell death cells, autoimmune diseases. Additionally, it summarizes key targets such as GPX4 TFR, responses. Furthermore, release multiple molecules, including damage-associated molecular patterns (DAMPs), following by is examined, these molecules further influence differentiation function thereby affecting occurrence progression Moreover, secrete factors or metabolites, which also impact target organs tissues involved Iron chelators, chloroquine its derivatives, antioxidants, calreticulin have been demonstrated to be effective animal studies for certain diseases, exerting anti-inflammatory immunomodulatory effects. Finally, brief summary future perspectives on are provided, aiming guide disease treatment strategies.
Language: Английский
Citations
9