Targeting hepatic oxidative stress rescues bone loss in liver fibrosis

Sonoda, Soichiro; Murata, Sara; Yamaza, Haruyoshi; Yuniartha, Ratih; Fujiyoshi, Junko; Yoshimaru, Koichiro; Matsuura, Toshiharu; Oda, Yoshinao; Ohga, Shouichi; Tajiri, Tasturo; Taguchi, Tomoaki; Yamaza, Takayoshi

doi:10.1016/j.molmet.2022.101599

Cited by 4 publications

(4 citation statements)

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“…Oxidative stress suppresses the osteogenic function and increases the osteoclastogenic capacity of BMMSCs 27 . To investigate the paracrine activity of PDLSCs, the osteogenic capacity of H 2 O 2 -ABSCs was then analyzed under CM-PDLSC stimulation.…”

Section: Resultsmentioning

confidence: 99%

“…6 a–d). RT-qPCR showed that local non-Tx enhanced the gingival receptor activator of nuclear factor κB ( Rank ) expression, which contributed to osteoclastic bone loss in periodontitis and oxidative stress 27 , 28 Local siCONT-PDLSC-Tx suppressed gingival Rank expression around the maxillary second molar, whereas local siEPOR-PDLSC-Tx did not, compared to the non-Tx group (Fig. 6 e).…”

Section: Resultsmentioning

confidence: 99%

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Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease

Zakaria,

Sonoda,

Kato

et al. 2024

Sci Rep

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Alveolar bone loss caused by periodontal disease eventually leads to tooth loss. Periodontal ligament stem cells (PDLSCs) are the tissue-specific cells for maintaining and repairing the periodontal ligament, cementum, and alveolar bone. Here, we investigated the role of erythropoietin receptor (EPOR), which regulates the microenvironment-modulating function of mesenchymal stem cells, in PDLSC-based periodontal therapy. We isolated PDLSCs from patients with chronic periodontal disease and healthy donors, referred to as PD-PDLSCs and Cont-PDLSCs, respectively. PD-PDLSCs exhibited reduced potency of periodontal tissue regeneration and lower expression of EPOR compared to Cont-PDLSCs. EPOR-silencing suppressed the potency of Cont-PDLSCs mimicking PD-PDLSCs, whereas EPO-mediated EPOR activation rejuvenated the reduced potency of PD-PDLSCs. Furthermore, we locally transplanted EPOR-silenced and EPOR-activated PDLSCs into the gingiva around the teeth of ligament-induced periodontitis model mice and demonstrated that EPOR in PDLSCs participated in the regeneration of the periodontal ligament, cementum, and alveolar bone in the ligated teeth. The EPOR-mediated paracrine function of PDLSCs maintains periodontal immune suppression and bone metabolic balance via osteoclasts and osteoblasts in the periodontitis model mice. Taken together, these results suggest that EPOR signaling is crucial for PDLSC-based periodontal regeneration and paves the way for the development of novel options for periodontal therapy.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease

Zakaria,

Sonoda,

Kato

et al. 2024

Sci Rep

Self Cite

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“…In addition, IL-1β can activate macrophages to produce IL-17 and promote liver fibrosis ( 111 ). IL-17 is widely expressed in portal regions, with evident inflammatory cell infiltration in liver tissues of patients with AIH ( 112 ), PBC ( 113 ), and overlap syndrome ( 114 ), and it is considered a significant proinflammatory and profibrotic agent in the liver ( 115 , 116 ). Accordingly, hepatic macrophage activation of Gal3/NLRP3 inflammasome/IL-17 signaling may be an additional significant pathogenic mechanism of PBC fibrosis ( 117 ).…”

Section: Inflammasomes and Pyroptosis In Aildsmentioning

confidence: 99%

Inflammasome and pyroptosis in autoimmune liver diseases

et al. 2023

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Autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and IgG4-related sclerosing cholangitis (IgG4-SC) are the four main forms of autoimmune liver diseases (AILDs), which are all defined by an aberrant immune system attack on the liver. Most previous studies have shown that apoptosis and necrosis are the two major modes of hepatocyte death in AILDs. Recent studies have reported that inflammasome-mediated pyroptosis is critical for the inflammatory response and severity of liver injury in AILDs. This review summarizes our present understanding of inflammasome activation and function, as well as the connections among inflammasomes, pyroptosis, and AILDs, thus highlighting the shared features across the four disease models and gaps in our knowledge. In addition, we summarize the correlation among NLRP3 inflammasome activation in the liver-gut axis, liver injury, and intestinal barrier disruption in PBC and PSC. We summarize the differences in microbial and metabolic characteristics between PSC and IgG4-SC, and highlight the uniqueness of IgG4-SC. We explore the different roles of NLRP3 in acute and chronic cholestatic liver injury, as well as the complex and controversial crosstalk between various types of cell death in AILDs. We also discuss the most up-to-date developments in inflammasome- and pyroptosis-targeted medicines for autoimmune liver disorders.

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“…Traditional Chinese medicine (TCM), as a unique medical approach in China, has better safety and effectiveness and is widely used to treat hepatic fibrosis[ 6 ]. Continuous oxidative stress (OS) in the liver can induce biological changes in hepatocytes, leading to fibrotic changes in the liver[ 7 ]. Based on this, experts and scholars have conducted relevant experimental studies to demonstrate that TCM monomers, single herbal extracts, and TCM formulas can significantly improve the condition of hepatic fibrosis by regulating OS.…”

Section: Introductionmentioning

confidence: 99%

Progress on traditional Chinese medicine in improving hepatic fibrosis through inhibiting oxidative stress

Li,

Zhu,

Ouyang

2023

World J Hepatol

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Patients with liver cirrhosis are advised to limit their sodium consumption to control excessive fluid accumulation. Salt is the most common form in which sodium is consumed daily. Consequently, various recommendations urge patients to limit salt intake. However, there is a lack of consistency regarding salt restriction across the guidelines. Moreover, there is conflicting evidence regarding the efficacy of salt restriction in the treatment of ascites. Numerous studies have shown that there is no difference in ascites control between patients with restriction of salt intake and those without restriction. Moreover, patients with cirrhosis may have several negative effects from consuming too little salt, although there are no recommendations on the lower limit of salt intake. Sodium is necessary to maintain the extracellular fluid volume; hence, excessive salt restriction can result in volume contraction, which could negatively impact kidney function in a cirrhotic patient. Salt restriction in cirrhotic patients can also compromise nutrient intake, which can have a negative impact on the overall outcome. There is insufficient evidence to recommend restricted salt intake for all patients with cirrhosis, including those with severe hyponatremia. The existing guidelines on salt restriction do not consider the salt sensitivity of patients; their nutritional state, volume status and sodium storage sites; and the risk of hypochloremia. This opinion article aims to critically analyze the existing literature with regard to salt recommendations for patients with liver cirrhosis and identify potential knowledge gaps that call for further research.

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Targeting hepatic oxidative stress rescues bone loss in liver fibrosis

Cited by 4 publications

References 49 publications

Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease

Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease

Inflammasome and pyroptosis in autoimmune liver diseases

Progress on traditional Chinese medicine in improving hepatic fibrosis through inhibiting oxidative stress

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