Cellular Signalling, Journal Year: 2024, Volume and Issue: 123, P. 111338 - 111338
Published: Aug. 6, 2024
Language: Английский
Frontiers in Medicine, Journal Year: 2025, Volume and Issue: 11
Published: Jan. 13, 2025
Gene therapy has long been a cornerstone in the treatment of rare diseases and genetic disorders, offering targeted solutions to conditions once considered untreatable. As field advances, its transformative potential is now expanding into oncology, where personalized therapies address immune-related complexities cancer. This review highlights innovative therapeutic strategies, including gene replacement, silencing, oncolytic virotherapy, CAR-T cell therapy, CRISPR-Cas9 editing, with focus on their application both hematologic malignancies solid tumors. CRISPR-Cas9, revolutionary tool precision medicine, enables precise editing cancer-driving mutations, enhancing immune responses disrupting tumor growth mechanisms. Additionally, emerging approaches target ferroptosis—a regulated, iron-dependent form death—offering new possibilities for selectively inducing death resistant cancers. Despite significant breakthroughs, challenges such as heterogeneity, evasion, immunosuppressive microenvironment (TME) remain. To overcome these barriers, novel like dual-targeting, armored cells, combination checkpoint inhibitors ferroptosis inducers are being explored. rise allogeneic “off-the-shelf” offers scalable more accessible options. The regulatory landscape evolving accommodate advancements, frameworks RMAT (Regenerative Medicine Advanced Therapy) U.S. ATMP (Advanced Therapy Medicinal Products) Europe fast-tracking approval therapies. However, ethical considerations surrounding CRISPR-based editing—such off-target effects, germline ensuring equitable access—remain at forefront, requiring ongoing oversight. Advances non-viral delivery systems, lipid nanoparticles (LNPs) exosomes, improving safety efficacy By integrating innovations addressing concerns, poised revolutionize cancer treatment, providing durable, effective,
Language: Английский
Citations
3
MedComm, Journal Year: 2025, Volume and Issue: 6(3)
Published: Feb. 23, 2025
Ferroptosis is a distinct form of iron-dependent programmed cell death characterized primarily by intracellular iron accumulation and lipid peroxidation. Multiple cellular processes, including amino acid metabolism, various signaling pathways, autophagy, have been demonstrated to influence the induction progression ferroptosis. Recent investigations elucidated that ferroptosis plays crucial role in pathogenesis pulmonary disorders, lung injury, chronic obstructive disease, fibrosis, asthma. increasingly recognized as promising novel strategy for cancer treatment. Various immune cells within tumor microenvironment, CD8+ T cells, macrophages, regulatory natural killer dendritic shown induce modulate process through regulation metabolism pathways. Conversely, can reciprocally alter metabolic environment, leading activation or inhibition functions, thereby modulating responses. This paper reviews molecular mechanism describes discusses connection between microenvironment diseases, development prospect their interaction treatment diseases.
Language: Английский
Citations
3
Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)
Published: Sept. 28, 2024
Language: Английский
Citations
17
Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 1012 - 1012
Published: Aug. 20, 2024
Oxidative stress (OS) is a key factor in the generation of various pathophysiological conditions. Nuclear erythroid 2 (NF-E2)-related (Nrf2) major transcriptional regulator antioxidant reactions. Heme oxygenase-1 (HO-1), gene regulated by Nrf2, one most critical cytoprotective molecules. In recent years, Nrf2/HO-1 has received widespread attention as regulatory pathway for intracellular defense against oxidative stress. It considered potential target treatment inflammatory bowel disease (IBD). This review highlights mechanism action and therapeutic significance IBD complications (intestinal fibrosis colorectal cancer (CRC)), well phytochemicals targeting IBD. The results suggest that effects on mainly involve following aspects: (1) Controlling to reduce intestinal inflammation injury; (2) Regulation flora repair mucosal barrier; (3) Prevention ferroptosis epithelial cells. However, due complex role Nrf2/HO-1, more nuanced understanding exact mechanisms involved way forward future.
Language: Английский
Citations
8
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: Jan. 23, 2025
Ferroptosis is a novel form of cell death distinct from traditional mechanisms, characterized by the accumulation iron ions and production lipid peroxides. It not only affects survival tumor cells but also closely linked to changes in microenvironment. Lung cancer one leading malignancies worldwide terms incidence mortality, its complex biological mechanisms resistance make treatment challenging. Recent studies have shown that ferroptosis plays key role onset progression lung cancer, with intricate regulatory influencing development response therapy. As research into deepens, related molecular pathways, such as glutamate metabolism, antioxidant defense, been gradually revealed. However, clinical practice, ferroptosis-based therapeutic strategies for are still their early stages. Challenges remain, including incomplete understanding specific ferroptosis, insufficient on factors, limited insight interactions within Therefore, effective modulation enhance remains an urgent issue. This review summarizes analyzes factors interaction microenvironment, further explores potential targeting ferroptosis. By synthesizing latest research, this paper aims provide new perspectives directions treatment, goal advancing applications.
Language: Английский
Citations
0
Cancer Letters, Journal Year: 2024, Volume and Issue: unknown, P. 217392 - 217392
Published: Dec. 1, 2024
Language: Английский
Citations
1
Cellular Signalling, Journal Year: 2024, Volume and Issue: 123, P. 111338 - 111338
Published: Aug. 6, 2024
Language: Английский
Citations
0