Pyroptosis: a double-edged sword in lung cancer and other respiratory diseases

Liang, Xiao; Qin, Ya; Wu, Dan; Wang, Qiong; Wu, Hongshuai

doi:10.1186/s12964-023-01458-w

Cited by 10 publications

(1 citation statement)

References 101 publications

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“…Active caspase-1 can cleave inactive forms of the pro-inflammatory cytokines of interleukin-1 beta (IL-1β) and IL-18 into their active forms [ 8 ]. Furthermore, inflammasome activation is linked to pyroptosis, a specific form of cell death mediated by gasdermin family proteins [ 9 ]. With the exception of AIM2, other inflammasomes such as NLRP1, NLRP3, and NLRC4 belong to NLRs Fig.…”

Section: Introductionmentioning

confidence: 99%

The interaction of inflammasomes and gut microbiota: novel therapeutic insights

Manshouri,

Seif,

Kamali

et al. 2024

Cell Commun Signal

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Inflammasomes are complex platforms for the cleavage and release of inactivated IL-1β and IL-18 cytokines that trigger inflammatory responses against damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs). Gut microbiota plays a pivotal role in maintaining gut homeostasis. Inflammasome activation needs to be tightly regulated to limit aberrant activation and bystander damage to the host cells. Several types of inflammasomes, including Node-like receptor protein family (e.g., NLRP1, NLRP3, NLRP6, NLRP12, NLRC4), PYHIN family, and pyrin inflammasomes, interact with gut microbiota to maintain gut homeostasis. This review discusses the current understanding of how inflammasomes and microbiota interact, and how this interaction impacts human health. Additionally, we introduce novel biologics and antagonists, such as inhibitors of IL-1β and inflammasomes, as therapeutic strategies for treating gastrointestinal disorders when inflammasomes are dysregulated or the composition of gut microbiota changes.

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Section: Introductionmentioning

confidence: 99%

The interaction of inflammasomes and gut microbiota: novel therapeutic insights

Manshouri,

Seif,

Kamali

et al. 2024

Cell Commun Signal

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Postoperative Injection of a Triptolide‐Preloaded Hydrogel Prevents the Recurrence of Glioblastoma by Dual‐Pathway Activation of Ferroptosis

Wu,

Cao,

Wang

et al. 2024

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Glioblastoma (GBM) recurrence leads to high mortality, which remains a major concern in clinical therapy. Herein, an injectable triptolide (TP)‐preloaded hydrogel (TP@DNH) accompanied by a postoperative injection strategy is developed to prevent the recurrence of GBM. With a potential inhibitor of the NRF2/SLC7A11/GPX4 axis, it is demonstrated that TP can deactivate glutathione peroxidase 4 (GPX4) from the source of glutathione (GSH) biosynthesis, thereby activating ferroptosis in GBM cells by blocking the neutralization of intracellular lipid peroxide (LPO). Based on acid‐sensitive Fe3+/tannic acid (TA) metal‐phenolic networks (MPNs), the TP@DNH hydrogel can induce the effective generation of reactive oxygen species (ROS) through Fe3+/TA‐mediated Fenton reaction and achieve controllable release of TP in resected GBM cavity. Due to ROS generation and GPX4 deactivation, postoperative injection of TP@DNH can achieve high‐level ferroptosis through dual‐pathway LPO accumulation, remarkably suppressing the growth of recurrent GBM and prolonging the overall survival in orthotopic GBM relapse mouse model. This work provides an alternative paradigm for regulating ferroptosis in the postoperative treatment of GBM.

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A new perspective on targeting pulmonary arterial hypertension: Programmed cell death pathways (Autophagy, Pyroptosis, Ferroptosis)

Ge,

Zhang,

et al. 2024

Biomedicine & Pharmacotherapy

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Pyroptosis: a double-edged sword in lung cancer and other respiratory diseases

Cited by 10 publications

References 101 publications

The interaction of inflammasomes and gut microbiota: novel therapeutic insights

The interaction of inflammasomes and gut microbiota: novel therapeutic insights

Postoperative Injection of a Triptolide‐Preloaded Hydrogel Prevents the Recurrence of Glioblastoma by Dual‐Pathway Activation of Ferroptosis

A new perspective on targeting pulmonary arterial hypertension: Programmed cell death pathways (Autophagy, Pyroptosis, Ferroptosis)

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