Targeting Programmed Cell Death to Improve Stem Cell Therapy: Implications for Treating Diabetes and Diabetes-Related Diseases

Zhāng, Qí; Wan, Xinxing; Hu, Xi-Min; Zhao, Wenjuan; Ban, Xiao-Xia; Huang, Yanxia; Yan, Weitao; Xiong, Kun

doi:10.3389/fcell.2021.809656

Cited by 15 publications

(6 citation statements)

References 145 publications

(159 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ferroptosis was the most recently coined form of regulated cell death, following the discovery of apoptosis ( Kerr et al, 1972 ), necrosis ( Galluzzi et al, 2017 ), and pyroptosis ( Galluzzi et al, 2018 ; Hu et al, 2021 ). In the past 10 years, multiple roles of ferroptosis in health and disease have been confirmed ( Dixon and Stockwell, 2019 ; Han et al, 2020 ; Li et al, 2020 ; van Swelm et al, 2020 ; Chen et al, 2021c ; Zhang et al, 2021b ). The number of publications related to ferroptosis was growing exponentially, especially in the field of cancer research ( Figure 1 ; Table 1 ) ( Chen et al, 2021b ; Jiang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

The Research Landscape of Ferroptosis in Cancer: A Bibliometric Analysis

Liang

Yang

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Background: Ferroptosis is a novel mechanism of programmed cell death coined in 2012, which has been found to play important roles in human health and disease. In the past decade, ferroptosis research has seen booming growth worldwide. The aim of this study was to visualize the scientific outputs and research trends of ferroptosis in the field of cancer.Methods: The raw data of publications were retrieved from the Web of Science Core Collection on 19 December 2021. The information on the impact factor (IF) and Journal Citation Reports (JCR) division were obtained from the website of Web of Science. Two kinds of software (CiteSpace and VOSviewer) were used to perform visualized analysis.Results: From 2012 to 2021, a total of 1833 publications related to ferroptosis in cancer were identified for final analysis. The annual number of citations and publications grew exponentially over the past decade. China (1,092) and United States (489) had the highest number of publications; Central South University and Guangzhou Medical University were the most productive institutions. Daolin Tang and Scott J Dixon were the most active authors ranked by most productive and co-cited, respectively. The journals with the highest output and co-citation frequency were Biochemical and Biophysical Research Communications and Cell, respectively. Among the 1833 publications, four were identified with citations more than 1000 times. Six co-cited references had a citation burst duration until 2021. Analysis of keywords suggested the current research of ferroptosis in cancer clusters in 9 hotspots and newly emerging frontier may be “multidrug resistance”.Conclusion: Cancer research is the major area of active research in ferroptosis. Our results provide a global landscape of the ferroptosis research in cancer from 2012 to 2021, which serves as a reference for future studies in this field.

show abstract

Section: Discussionmentioning

confidence: 99%

The Research Landscape of Ferroptosis in Cancer: A Bibliometric Analysis

Liang

Yang

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…Besides the immune problem, the logarithmic increase in the global population of people with diabetes, the limited donor supply, and the need for lifelong immunosuppression restrict its widespread use (25). Numerous therapeutic approaches have been reported to solve this problem, including the search for bcell substitutes, porcine islet xenotransplantation, and stem cell transplantations, which present solutions to the donor shortage and may be the most likely alternatives (26,27).…”

Section: The Difficulties Of Insulin Replacement and B-cell Replaceme...mentioning

confidence: 99%

Stem Cell Transplantation in the Treatment of Type 1 Diabetes Mellitus: From Insulin Replacement to Beta-Cell Replacement

et al. 2022

Self Cite

View full text Add to dashboard Cite

Type 1 diabetes mellitus (T1DM) is an autoimmune disease that attacks pancreatic β-cells, leading to the destruction of insulitis-related islet β-cells. Islet β-cell transplantation has been proven as a curative measure in T1DM. However, a logarithmic increase in the global population with diabetes, limited donor supply, and the need for lifelong immunosuppression restrict the widespread use of β-cell transplantation. Numerous therapeutic approaches have been taken to search for substitutes of β-cells, among which stem cell transplantation is one of the most promising alternatives. Stem cells have demonstrated the potential efficacy to treat T1DM by reconstitution of immunotolerance and preservation of islet β-cell function in recent research. cGMP-grade stem cell products have been used in human clinical trials, showing that stem cell transplantation has beneficial effects on T1DM, with no obvious adverse reactions. To better achieve remission of T1DM by stem cell transplantation, in this work, we explain the progression of stem cell transplantation such as mesenchymal stem cells (MSCs), human embryonic stem cells (hESCs), and bone marrow hematopoietic stem cells (BM-HSCs) to restore the immunotolerance and preserve the islet β-cell function of T1DM in recent years. This review article provides evidence of the clinical applications of stem cell therapy in the treatment of T1DM.

show abstract

“…The NLRP3 inflammasome increased in the procession of sepsis and functioned as the key regulator of pyroptosis [37][38][39]. Pyroptosis, playing a protective role in host defense during infection, is an inflammatory form of regulated cell death (RCD) [40][41][42][43][44][45]. Mature IL-1β is cleaved by the activated NLRP3/caspase1 pathway, and the cleaved IL-1β is released through the pore in the cell membrane and induces pyroptosis [46][47][48].…”

Section: Introductionmentioning

confidence: 99%

HSF1 Alleviates Brain Injury by Inhibiting NLRP3-Induced Pyroptosis in a Sepsis Model

et al. 2023

Mediators of Inflammation

Self Cite

View full text Add to dashboard Cite

Background. Sepsis, which could cause a systemic inflammatory response, is a life-threatening disease with a high morbidity and mortality rate. There is evidence that brain injury may be related to severe systemic infection induced by sepsis. The brain injury caused by sepsis could increase the risk of mortality in septic patients, which seriously affects the septic patient’s prognosis of survival. Although there remains a focus on sepsis research, clinical measures to prevent and treat brain injury in sepsis are not yet available, and the high mortality rate is still a big health burden. Therefore, it is necessary to investigate the new molecules or regulated pathways that can effectively inhibit the progress of sepsis. Objective. NLR family pyrin domain-containing 3 (NLRP3) increased in the procession of sepsis and functioned as the key regulator of pyroptosis. Heat shock factor 1 (HSF1) can protect organs from multiorgan dysfunction syndrome induced by lipopolysaccharides in mice, and NLRP3 could be inhibited by HSF1 in many organs. However, whether HSF1 regulated NLRP3 in sepsis-induced brain injury, as well as the detailed mechanism of HSF1 in brain injury, remains unknown in the sepsis model. In this research, we try to explore the relationship between HSF1 and NLRP3 in a sepsis model and try to reveal the mechanism of HSF1 inhibiting the process of brain injury. Methods. In this study, we used wild-type mice and hsf1-/- mice for in vivo research and PC12 cells for in vitro research. Real-time PCR and Western blot were used to analyze the expression of HSF1, NLRP3, cytokines, and pyrolytic proteins. EthD-III staining was chosen to detect the pyroptosis of the hippocampus and PC12 cells. Results. The results showed that HSF1 is negatively related to pyroptosis. The pyroptosis in cells of brain tissue was significantly increased in the hsf1-/- mouse model compared to hsf1+/+ mice. In PC12 cells, hsf1 siRNA can upregulate pyroptosis while HSF1-transfected plasmid could inhibit the pyroptosis. HSF1 could negatively regulate the NLRP3 pathway in PC12 cells, while hsf1 siRNA enhanced the pyroptosis in PC12 cells, which could be reversed by nlrp3 siRNA. Conclusion. These results imply that HSF1 could alleviate sepsis-induced brain injury by inhibiting pyroptosis through the NLRP3-dependent pathway in brain tissue and PC12 cells, suggesting HSF1 as a potential molecular target for treating brain injury in sepsis clinical studies.

show abstract

Targeting Programmed Cell Death to Improve Stem Cell Therapy: Implications for Treating Diabetes and Diabetes-Related Diseases

Cited by 15 publications

References 145 publications

The Research Landscape of Ferroptosis in Cancer: A Bibliometric Analysis

The Research Landscape of Ferroptosis in Cancer: A Bibliometric Analysis

Stem Cell Transplantation in the Treatment of Type 1 Diabetes Mellitus: From Insulin Replacement to Beta-Cell Replacement

HSF1 Alleviates Brain Injury by Inhibiting NLRP3-Induced Pyroptosis in a Sepsis Model

Contact Info

Product

Resources

About