Celastrol relieves myocardial infarction-induced cardiac fibrosis by inhibiting NLRP3 inflammasomes in rats

Fan, Jiwen; Ren, Meng; Chen, Weiwei; Wang, Haodong; He, Yuquan

doi:10.1016/j.intimp.2023.110511

Cited by 7 publications

(2 citation statements)

References 37 publications

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“…Herbal medicines have been widely utilized alone or as a supplement and alternative therapy to treat various disorders in East Asia because of their reduced toxicity, fewer side effects, and cheaper cost ( 84 ). Many herbal ingredients may act synergistically to protect against myocardial injury in IHD through suppressing NR, such as salvianolic acid b, stigmasterol, resveratrol ( 85 ), tetrandrine ( 86 ), baicalin ( 87 ), silibinin ( 88 ), 2-methoxycinnamaldehyde ( 89 ), celastrol ( 90 ), et al. ( Table 3 ).…”

Section: Interventions To Regulate Nrmentioning

confidence: 99%

Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment

Wang,

Shou,

et al. 2024

Front. Immunol.

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Ischemic heart disease (IHD) can trigger responses from the innate immune system, provoke aseptic inflammatory processes, and result in the recruitment and accumulation of neutrophils. Excessive recruitment of neutrophils is a potential driver of persistent cardiac inflammation. Once recruited, neutrophils are capable of secreting a plethora of inflammatory and chemotactic agents that intensify the inflammatory cascade. Additionally, neutrophils may obstruct microvasculature within the inflamed region, further augmenting myocardial injury in the context of IHD. Immune-related molecules mediate the recruitment process of neutrophils, such as immune receptors and ligands, immune active molecules, and immunocytes. Non-immune-related molecular pathways represented by pro-resolving lipid mediators are also involved in the regulation of NR. Finally, we discuss novel regulating strategies, including targeted intervention, agents, and phytochemical strategies. This review describes in as much detail as possible the upstream molecular mechanism and external intervention strategies for regulating NR, which represents a promising therapeutic avenue for IHD.

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Section: Interventions To Regulate Nrmentioning

confidence: 99%

Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment

Wang,

Shou,

et al. 2024

Front. Immunol.

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“…Luo et al, 2023), heart failure (HF) (J. Wang, Tomar, et al, 2023) and myocardial infraction (Fan et al, 2023). A variety of inflammasomes (NLRP3 [NOD-like receptor thermal protein domain associated protein 3], NLRP1, AIM2 [absent in melanoma 2] and NLRC4) have been linked to the development of cardiocerebrovascular diseases, and blocking these multiprotein complexes presents as a potential therapeutic target for disease regulation with only mild immunodeficiency side effects (Borborema et al, 2020;Deng et al, 2023;Shao et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

The cytoplasmic sensor, the AIM2 inflammasome: A precise therapeutic target in vascular and metabolic diseases

Lin,

Wang,

Fang

et al. 2024

British J Pharmacology

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Cardio‐cerebrovascular diseases encompass pathological changes in the heart, brain and vascular system, which pose a great threat to health and well‐being worldwide. Moreover, metabolic diseases contribute to and exacerbate the impact of vascular diseases. Inflammation is a complex process that protects against noxious stimuli but is also dysregulated in numerous so‐called inflammatory diseases, one of which is atherosclerosis. Inflammation involves multiple organ systems and a complex cascade of molecular and cellular events. Numerous studies have shown that inflammation plays a vital role in cardio‐cerebrovascular diseases and metabolic diseases. The absent in melanoma 2 (AIM2) inflammasome detects and is subsequently activated by double‐stranded DNA in damaged cells and pathogens. With the assistance of the mature effector molecule caspase‐1, the AIM2 inflammasome performs crucial biological functions that underpin its involvement in cardio‐cerebrovascular diseases and related metabolic diseases: The production of interleukin‐1 beta (IL-1β), interleukin‐18 (IL-18) and N‐terminal pore‐forming Gasdermin D fragment (GSDMD‐N) mediates a series of inflammatory responses and programmed cell death (pyroptosis and PANoptosis). Currently, several agents have been reported to inhibit the activity of the AIM2 inflammasome and have the potential to be evaluated for use in clinical settings. In this review, we systemically elucidate the assembly, biological functions, regulation and mechanisms of the AIM2 inflammasome in cardio‐cerebrovascular diseases and related metabolic diseases and outline the inhibitory agents of the AIM2 inflammasome as potential therapeutic drugs.

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Celastrol alleviates subconjunctival fibrosis induced by silicone implants mimicking glaucoma surgery

Wang,

Geng,

Sun

et al. 2024

European Journal of Pharmaceutics and Biopharmaceutics

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Celastrol relieves myocardial infarction-induced cardiac fibrosis by inhibiting NLRP3 inflammasomes in rats

Cited by 7 publications

References 37 publications

Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment

Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment

The cytoplasmic sensor, the AIM2 inflammasome: A precise therapeutic target in vascular and metabolic diseases

Celastrol alleviates subconjunctival fibrosis induced by silicone implants mimicking glaucoma surgery

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