Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases

Chen, Yonghu; Zhang, Yuqi; Li, Ning; Zhe, Jiang; Li, Xuezheng

doi:10.1007/s00011-023-01712-4

Cited by 10 publications

(6 citation statements)

References 147 publications

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“…Moreover, IL-1β promotes ROS accumulation, which in turn stimulates the activation of NLRP3 inflammasome, resulting in the formation of more IL-1β and initiation of a feedback loop between the activation of NLRP3 inflammasome and oxidative stress. 40–42 Our study revealed the activation of NLRP3 inflammasome pathway in the BLM group indicated by an increased NLPP3, ASC, caspase-1, and IL-1β, which is in line with previous studies 39,43 that demonstrate the activation of NLRP3 inflammasome after instillation of BLM. Contrariwise, the enhanced NLPP3, ASC, caspase-1, and IL-1β in BLM rats were attenuated after BET administration.…”

Section: Discussionsupporting

confidence: 91%

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Abd Elrazik,

Helmy

2024

Food Funct.

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Section: Discussionsupporting

confidence: 91%

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Abd Elrazik,

Helmy

2024

Food Funct.

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“…Cholestasis is a pathological state in which bile flow cannot enter the duodenum and enter the blood instead due to the obstruction of bile formation, secretion and excretion caused by various reasons [18]. The pathological changes of ACLF are one-time (or multiple) necrosis of hepatocytes, which can be manifested as mass necrosis (the necrosis scope exceeds 2/3 of the hepatic parenchyma), and sub-mass necrosis (about 1/2 ~ 2/3 of the hepatic parenchyma) [19].…”

Section: Metabolism Of Ba and Their Toxic Effects On Hepatocytesmentioning

confidence: 99%

Exploring the interaction between bile acid and intestinal microbiota in acute-on-chronic liver failure and the progress of treatment strategies

Zeng,

Gan,

Zeng

et al. 2024

J Gastroenterol Res Pract

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Acute-on-Chronic Liver Failure (ACLF) is an acute and severe disease involving single or multiple organ failure. Due to the unclear pathogenesis, there is still a lack of effective drug treatment. Intestinal microbiota is closely related to Bile Acid (BA) metabolism. In the progression of chronic liver disease to ACLF, BA metabolism disorder is often accompanied by intestinal microbiota imbalance, which affect one another mutually. This article reviewed the role of BA metabolism and intestinal microbiota in the progression of ACLF, which aims to explore potential new targets for the treatment of ACLF.

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“…The inflammasome plays a crucial role in the pathogenesis of acute and chronic respiratory diseases [77]. As in other organ-specific disorders, the NLRP3 inflammasome is first activated by microbial agents, then followed by a second signal that can be triggered by a wide range of factors acting as DAMPs such as extracellular ATP, toxins, RNA viruses, ion flow, mitochondrial dysfunction, ROS, or lysosomal damage, all occurring during pulmonary inflammation.…”

Section: Inflammasome Involvement In Pulmonary Diseasesmentioning

confidence: 99%

NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases—A Lesson from Cytokine Storm Syndrome

Napodano,

Carnazzo,

Basile

et al. 2023

IJMS

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Inflammation and inflammasomes have been proposed as important regulators of the host–microorganism interaction, playing a key role in morbidity and mortality due to the coronavirus disease 2019 (COVID-19) in subjects with chronic conditions and compromised immune system. The inflammasome consists of a multiprotein complex that finely regulates the activation of caspase-1 and the production and secretion of potent pro-inflammatory cytokines such as IL-1β and IL-18. The pyrin containing NOD (nucleotide-binding oligomerization domain) like receptor (NLRP) is a family of intracellular receptors, sensing patterns associated to pathogens or danger signals and NLRP3 inflammasome is the most deeply analyzed for its involvement in the innate and adaptive immune system as well as its contribution to several autoinflammatory and autoimmune diseases. It is highly expressed in leukocytes and up-regulated in sentinel cells upon inflammatory stimuli. NLRP3 expression has also been reported in B and T lymphocytes, in epithelial cells of oral and genital mucosa, in specific parenchymal cells as cardiomyocytes, and keratinocytes, and chondrocytes. It is well known that a dysregulated activation of the inflammasome is involved in the pathogenesis of different disorders that share the common red line of inflammation in their pathogenetic fingerprint. Here, we review the potential roles of the NLRP3 inflammasome in cardiovascular events, liver damage, pulmonary diseases, and in that wide range of systemic inflammatory syndromes named as a cytokine storm.

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Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases

Cited by 10 publications

References 147 publications

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Betanin protects against bleomycin-induced pulmonary fibrosis by regulating the NLRP3/IL-1β/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition

Exploring the interaction between bile acid and intestinal microbiota in acute-on-chronic liver failure and the progress of treatment strategies

NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases—A Lesson from Cytokine Storm Syndrome

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