The scheme, and regulative mechanism of pyroptosis, ferroptosis, and necroptosis in radiation injury

Ning, Jiaoyang; Chen, Liu; Zeng, Yu; Xiao, Gang; Tian, Wentao; Wu, Qi; Tang, Jiyuan; He, Shuangshuang; Tanzhu, Guilong; Zhou, Rongrong

doi:10.7150/ijbs.91112

Cited by 4 publications

(1 citation statement)

References 141 publications

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“…Radiation therapy (RT) is the main treatment method for tumors, but it inevitably damage to normal cells. Ning et al (2024) found that some plant extracts, exosomes, and plasmids exhibited the repair of radiation-induced hematopoietic and skin damage by inhibiting ferroptosis; Melatonin promoted the binding of Nrf2 and pyruvate kinase isoenzyme M2 (PKM2), which reduced iron concentration and inhibited ferroptosis to alleviate radiation-induced hippocampal neuronal death. Yue et al (2024) summarized that various anti-tumor drugs such as cisplatin, paclitaxel, capecitabine, apatinib and artemisinin could induce ferroptosis in gastric cancer (GC) cells.…”

Section: Clinical Researches Progress Of Targeting Ferroptosis In The...mentioning

confidence: 99%

Ferroptosis: emerging roles in lung cancer and potential implications in biological compounds

Liang,

Wang,

et al. 2024

Front. Pharmacol.

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Lung cancer has high metastasis and drug resistance. The prognosis of lung cancer patients is poor and the patients’ survival chances are easily neglected. Ferroptosis is a programmed cell death proposed in 2012, which differs from apoptosis, necrosis and autophagy. Ferroptosis is a novel type of regulated cell death which is driven by iron-dependent lipid peroxidation and subsequent plasma membrane ruptures. It has broad prospects in the field of tumor disease treatment. At present, multiple studies have shown that biological compounds can induce ferroptosis in lung cancer cells, which exhibits significant anti-cancer effects, and they have the advantages in high safety, minimal side effects, and less possibility to drug resistance. In this review, we summarize the biological compounds used for the treatment of lung cancer by focusing on ferroptosis and its mechanism. In addition, we systematically review the current research status of combining nanotechnology with biological compounds for tumor treatment, shed new light for targeting ferroptosis pathways and applying biological compounds-based therapies.

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Section: Clinical Researches Progress Of Targeting Ferroptosis In The...mentioning

confidence: 99%

Ferroptosis: emerging roles in lung cancer and potential implications in biological compounds

Liang,

Wang,

et al. 2024

Front. Pharmacol.

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Metastatic brain tumors: from development to cutting‐edge treatment

Tanzhu,

Chen,

Ning

et al. 2024

MedComm

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Metastatic brain tumors, also called brain metastasis (BM), represent a challenging complication of advanced tumors. Tumors that commonly metastasize to the brain include lung cancer and breast cancer. In recent years, the prognosis for BM patients has improved, and significant advancements have been made in both clinical and preclinical research. This review focuses on BM originating from lung cancer and breast cancer. We briefly overview the history and epidemiology of BM, as well as the current diagnostic and treatment paradigms. Additionally, we summarize multiomics evidence on the mechanisms of tumor occurrence and development in the era of artificial intelligence and discuss the role of the tumor microenvironment. Preclinically, we introduce the establishment of BM models, detailed molecular mechanisms, and cutting‐edge treatment methods. BM is primarily treated with a comprehensive approach, including local treatments such as surgery and radiotherapy. For lung cancer, targeted therapy and immunotherapy have shown efficacy, while in breast cancer, monoclonal antibodies, tyrosine kinase inhibitors, and antibody–drug conjugates are effective in BM. Multiomics approaches assist in clinical diagnosis and treatment, revealing the complex mechanisms of BM. Moreover, preclinical agents often need to cross the blood–brain barrier to achieve high intracranial concentrations, including small‐molecule inhibitors, nanoparticles, and peptide drugs. Addressing BM is imperative.

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Mechanisms of radiation‐induced tissue damage and response

Zhou,

Zhu,

Liu

et al. 2024

MedComm

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Radiation‐induced tissue injury (RITI) is the most common complication in clinical tumor radiotherapy. Due to the heterogeneity in the response of different tissues to radiation (IR), radiotherapy will cause different types and degrees of RITI, which greatly limits the clinical application of radiotherapy. Efforts are continuously ongoing to elucidate the molecular mechanism of RITI and develop corresponding prevention and treatment drugs for RITI. Single‐cell sequencing (Sc‐seq) has emerged as a powerful tool in uncovering the molecular mechanisms of RITI and for identifying potential prevention targets by enhancing our understanding of the complex intercellular relationships, facilitating the identification of novel cell phenotypes, and allowing for the assessment of cell heterogeneity and spatiotemporal developmental trajectories. Based on a comprehensive review of the molecular mechanisms of RITI, we analyzed the molecular mechanisms and regulatory networks of different types of RITI in combination with Sc‐seq and summarized the targeted intervention pathways and therapeutic drugs for RITI. Deciphering the diverse mechanisms underlying RITI can shed light on its pathogenesis and unveil new therapeutic avenues to potentially facilitate the repair or regeneration of currently irreversible RITI. Furthermore, we discuss how personalized therapeutic strategies based on Sc‐seq offer clinical promise in mitigating RITI.

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The scheme, and regulative mechanism of pyroptosis, ferroptosis, and necroptosis in radiation injury

Cited by 4 publications

References 141 publications

Ferroptosis: emerging roles in lung cancer and potential implications in biological compounds

Ferroptosis: emerging roles in lung cancer and potential implications in biological compounds

Metastatic brain tumors: from development to cutting‐edge treatment

Mechanisms of radiation‐induced tissue damage and response

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