Heat Shock Transcription Factor 2 Promotes Mitophagy of Intestinal Epithelial Cells Through PARL/PINK1/Parkin Pathway in Ulcerative Colitis

Liang, Hao; Zhang, Fengrui; Wang, Wen; Zhao, Wei; Zhou, Jiao; Feng, Yuran; Wu, Jing; Li, Maojuan; Bai, Xinyu; Zeng, Zhong; Niu, Junkun; Miao, Yi

doi:10.3389/fphar.2022.893426

Cited by 9 publications

(4 citation statements)

References 32 publications

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“…The mice were randomly divided into control and DSS-treated groups of ten mice each, and the mice in the control group were given distilled water ad libitum for seven days, while the mice in the DSS-treated group were given DSS solution (MP Biomedicals, United States) at a concentration of 2 % ad libitum for seven days. The body weight, fecal characteristics, blood in stool, and DAI scores of the mice were recorded daily 21 . The mice were decapitated on the 8th day of modeling, and the colonic tissues were dissected and stored in a freezer at -80 °C.…”

Section: Methodsmentioning

confidence: 99%

Comprehensive analysis of disulfidptosis-related genes reveals the effect of disulfidptosis in ulcerative colitis

Song,

Zhang,

Bai

et al. 2024

Sci Rep

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Ulcerative colitis (UC) is a chronic inflammatory condition of the intestinal tract. Various programmed cell death pathways in the intestinal mucosa are crucial to the pathogenesis of UC. Disulfidptosis, a recently identified form of programmed cell death, has not been extensively reported in the context of UC. This study evaluated the expression of disulfidptosis-related genes (DRGs) in UC through public databases and assessed disulfide accumulation in the intestinal mucosal tissues of UC patients and dextran sulfate sodium (DSS)-induced colitis mice via targeted metabolomics. We utilized various bioinformatics techniques to identify UC-specific disulfidptosis signature genes, analyze their potential functions, and investigate their association with immune cell infiltration in UC. The mRNA and protein expression levels of these signature genes were confirmed in the intestinal mucosa of DSS-induced colitis mice and UC patients. A total of 24 DRGs showed differential expression in UC. Our findings underscore the role of disulfide stress in UC. Four UC-related disulfidptosis signature genes—SLC7A11, LRPPRC, NDUFS1, and CD2AP—were identified. Their relationships with immune infiltration in UC were analyzed using CIBERSORT, and their expression levels were validated by quantitative real-time PCR and western blotting. This study provides further insights into their potential functions and explores their links to immune infiltration in UC. In summary, disulfidptosis, as a type of programmed cell death, may significantly influence the pathogenesis of UC by modulating the homeostasis of the intestinal mucosal barrier.

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Section: Methodsmentioning

confidence: 99%

Comprehensive analysis of disulfidptosis-related genes reveals the effect of disulfidptosis in ulcerative colitis

Song,

Zhang,

Bai

et al. 2024

Sci Rep

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“…Mitophagy removes damaged mitochondria, thereby reducing the mitochondrial ROS and subsequently preventing the induction of the NLRP3 inflammasome by ROS. It has been observed that both the number of damaged mitochondria and mitophagy are increased in intestinal tissue from UC patients, and this correlates with disease severity [47]. In that study, the authors identified Heat Shock Transcription Factor 2 (HSF2) as a regulator of mitophagy through the PARL/PINK1/Parkin pathway.…”

Section: Mitochondrial Dynamics Mitophagy and Mitochondrial Biogenesi...mentioning

confidence: 99%

Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review

Sánchez-Quintero,

Rodríguez-Díaz,

Rodríguez-González

et al. 2023

IJMS

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Mitochondria are key cellular organelles whose main function is maintaining cell bioenergetics by producing ATP through oxidative phosphorylation. However, mitochondria are involved in a much higher number of cellular processes. Mitochondria are the home of key metabolic pathways like the tricarboxylic acid cycle and β-oxidation of fatty acids, as well as biosynthetic pathways of key products like nucleotides and amino acids, the control of the redox balance of the cell and detoxifying the cell from H2S and NH3. This plethora of critical functions within the cell is the reason mitochondrial function is involved in several complex disorders (apart from pure mitochondrial disorders), among them inflammatory bowel diseases (IBD). IBD are a group of chronic, inflammatory disorders of the gut, mainly composed of ulcerative colitis and Crohn’s disease. In this review, we present the current knowledge regarding the impact of mitochondrial dysfunction in the context of IBD. The role of mitochondria in both intestinal mucosa and immune cell populations are discussed, as well as the role of mitochondrial function in mechanisms like mucosal repair, the microbiota– and brain–gut axes and the development of colitis-associated colorectal cancer.

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“…In addition, mtROS not only directly regulates the assembly process of inflammasome, but also indirectly regulates the activity of inflammasome by affecting cytoplasmic proteins [ 43 ]. Specifically, mtROS mediates the dissociation of thioredoxin-interacting protein (TXNIP) from thioredoxin and then interacts with NLRP3 protein to activate the NLRP3 inflammasome [ 44 ].…”

Section: Activation Mechanism Of the Nlrp3 Inflammasomementioning

confidence: 99%

The NLRP3 inflammasome: contributions to inflammation-related diseases

Cao

Escames

et al. 2023

Cell Mol Biol Lett

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The NOD-like receptor protein 3 (NLRP3) inflammasome is a protein complex that regulates innate immune responses by activating caspase-1 and the inflammatory cytokines interleukin (IL)-1β and IL-18. Multiple studies have demonstrated the importance of the NLRP3 inflammasome in the development of immune and inflammation-related diseases, including arthritis, Alzheimer’s disease, inflammatory bowel disease, and other autoimmune and autoinflammatory diseases. This review first explains the activation and regulatory mechanism of the NLRP3 inflammasome. Secondly, we focus on the role of the NLRP3 inflammasome in various inflammation-related diseases. Finally, we look forward to new methods for targeting the NLRP3 inflammasome to treat inflammation-related diseases, and provide new ideas for clinical treatment.

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Heat Shock Transcription Factor 2 Promotes Mitophagy of Intestinal Epithelial Cells Through PARL/PINK1/Parkin Pathway in Ulcerative Colitis

Cited by 9 publications

References 32 publications

Comprehensive analysis of disulfidptosis-related genes reveals the effect of disulfidptosis in ulcerative colitis

Comprehensive analysis of disulfidptosis-related genes reveals the effect of disulfidptosis in ulcerative colitis

Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review

The NLRP3 inflammasome: contributions to inflammation-related diseases

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