MiR-223-3p attenuates radiation-induced inflammatory response and inhibits the activation of NLRP3 inflammasome in macrophages

Zhang, Mingwei; Lan, Hailin; Peng, Shaoli; Zhou, Weitong; Wang, Xuezhen; Jiang, Meina; Hong, Jinsheng; Zhang, Qiuyu

doi:10.1016/j.intimp.2023.110616

Cited by 12 publications

(5 citation statements)

References 42 publications

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“… [ 54 ] GSDMD-mediated pyroptosis is induced in mouse macrophages after irradiation. [ 62 ] Microvascular endothelial cells undergo pyroptosis caused by GSDMD through gamma radiation. [ 23 ] GSDME GSDME is a critical determinant of radiosensitivity in nasopharyngeal carcinoma.…”

Section: Radiation Regulates Pyroptosis Through Various Mechanismsmentioning

confidence: 99%

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Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Li,

Yang,

Zhang

et al. 2024

Cell Death Discov.

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Pyroptotic cell death, an inflammatory form of programmed cell death (PCD), is emerging as a potential therapeutic opportunity for radiotherapy (RT). RT is commonly used for cancer treatment, but its effectiveness can be limited by tumor resistance and adverse effects on healthy tissues. Pyroptosis, characterized by cell swelling, membrane rupture, and release of pro-inflammatory cytokines, has been shown to enhance the immune response against cancer cells. By inducing pyroptotic cell death in tumor cells, RT has the potential to enhance treatment outcomes by stimulating anti-tumor immune responses and improving the overall efficacy of RT. Furthermore, the release of danger signals from pyroptotic cells can promote the recruitment and activation of immune cells, leading to a systemic immune response that may target distant metastases. Although further research is needed to fully understand the mechanisms and optimize the use of pyroptotic cell death in RT, it holds promise as a novel therapeutic strategy for improving cancer treatment outcomes. This review aims to synthesize recent research on the regulatory mechanisms underlying radiation-induced pyroptosis and to elucidate the potential significance of this process in RT. The insights gained from this analysis may inform strategies to enhance the efficacy of RT for tumors.

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Section: Radiation Regulates Pyroptosis Through Various Mechanismsmentioning

confidence: 99%

“…The main causes of ARILI are immune and inflammatory dysfunction [ 60 , 61 ]. miR-223-3p can improve radiation-induced macrophage pyroptosis and lung damage [ 62 ]. Macrophages play an important role in acute lung injury [ 63 ].…”

Section: Potential Therapeutic Application Of Rt-induced Pyroptosismentioning

confidence: 99%

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Li,

Yang,

Zhang

et al. 2024

Cell Death Discov.

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“…Thus, it can be inferred that MCP-1 plays a direct role in the stimulation and recruitment of macrophages. TNF-α might play a pivotal role in the pathogenesis of diet-induced NASH by activating inflammatory cells to exert its significant effects ( Kugelmas et al, 2003 ; Zhang et al, 2023 ). Similarly, IL-1β can promote the proliferation and transdifferentiation of hepatic stellate cells and is responsible for the accumulation of fibrotic tissue.…”

Section: The Role Of Pyroptosis In Nafldmentioning

confidence: 99%

The role and mechanism of pyroptosis and potential therapeutic targets in non-alcoholic fatty liver disease (NAFLD)

Li,

Liu,

et al. 2024

Front. Cell Dev. Biol.

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Non-alcoholic fatty liver disease (NAFLD) is a clinical pathological syndrome characterized by the excessive accumulation of fat within liver cells, which can progress to end-stage liver disease in severe cases, posing a threat to life. Pyroptosis is a distinct, pro-inflammatory form of cell death, differing from traditional apoptosis. In recent years, there has been growing research interest in the association between pyroptosis and NAFLD, encompassing the mechanisms and functions of pyroptosis in the progression of NAFLD, as well as potential therapeutic targets. Controlled pyroptosis can activate immune cells, eliciting host immune responses to shield the body from harm. However, undue activation of pyroptosis may worsen inflammatory responses, induce cellular or tissue damage, disrupt immune responses, and potentially impact liver function. This review elucidates the involvement of pyroptosis and key molecular players, including NOD-like receptor thermal protein domain associated protein 3(NLRP3) inflammasome, gasdermin D (GSDMD), and the caspase family, in the pathogenesis and progression of NAFLD. It emphasizes the promising prospects of targeting pyroptosis as a therapeutic approach for NAFLD and offers valuable insights into future directions in the field of NAFLD treatment.

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“…Regarding dose rates, 1-4 Gy/min is commonly applied. Zhang et al conducted a study using a high dose rate of 12.61 Gy/min to induce pyroptosis 96 . No distinct pattern emerges between cell death modes and cell/animal models.…”

Section: Introductionmentioning

confidence: 99%

“…IR-induced pyroptosis can influence radiation-induced damage development by modulating macrophages, dendritic cells, T cells, and natural killer cells (NK cells). Andrographolide (Figure 3 Aa) and miR-223-3p (Figure 3 Ab) inhibit caspase-1-mediated macrophage pyroptosis by targeting the AIM2 and NLRP3 inflammasomes, thereby mitigating radiation-induced lung injury 96 , 97 . The combination of RDN and IR effectively prevents pyroptosis and radiation pneumonitis.…”

Section: Introductionmentioning

confidence: 99%

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

Ning,

Chen,

Zeng

et al. 2024

Int. J. Biol. Sci.

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Radiotherapy (RT) stands as the primary treatment for tumors, but it inevitably causes damage to normal cells. Consequently, radiation injury is a crucial consideration for radiation oncologists during therapy planning. Cell death including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis play significant roles in tumor treatment. While previous studies elucidated the induction of apoptosis and autophagy by ionizing radiation (IR), recent attention has shifted to pyroptosis, ferroptosis, and necroptosis, revealing their effects induced by IR. This review aims to summarize the strategies employed by IR, either alone or in combination therapy, to induce pyroptosis, ferroptosis, and necroptosis in radiation injury. Furthermore, we explore their effects and molecular pathways, shedding light on their roles in radiation injury. Finally, we summarize the regulative agents for these three types of cell death and their mechanisms. In summary, optimizing radiation dose, dose rate, and combined treatment plans to minimize radiation damage and enhance the killing effect of RT is a key focus.

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MiR-223-3p attenuates radiation-induced inflammatory response and inhibits the activation of NLRP3 inflammasome in macrophages

Cited by 12 publications

References 42 publications

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

Pyroptotic cell death: an emerging therapeutic opportunity for radiotherapy

The role and mechanism of pyroptosis and potential therapeutic targets in non-alcoholic fatty liver disease (NAFLD)

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

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