Cytokine & Growth Factor Reviews最新文献_第10页

Acinar cells and the development of pancreatic fibrosis 腺泡细胞与胰腺纤维化的发生

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.05.003

Jianhong An , Tingting Jiang , Ling Qi , Keping Xie

{"title":"Acinar cells and the development of pancreatic fibrosis","authors":"Jianhong An , Tingting Jiang , Ling Qi , Keping Xie","doi":"10.1016/j.cytogfr.2023.05.003","DOIUrl":"10.1016/j.cytogfr.2023.05.003","url":null,"abstract":"<div>Pancreatic fibrosis is caused by excessive deposition of extracellular matrixes of collagen and fibronectin in the pancreatic tissue as a result of repeated injury often seen in patients with chronic pancreatic diseases. The most common causative conditions include inborn errors of metabolism, chemical toxicity and autoimmune disorders. Its pathophysiology is highly complex, including acinar cell injury, acinar stress response, duct dysfunction, pancreatic stellate cell activation, and persistent inflammatory response. However, the specific mechanism remains to be fully clarified. Although the current therapeutic strategies targeting pancreatic stellate cells show good efficacy in cell culture and animal models, they are not satisfactory in the clinic. Without effective intervention, pancreatic fibrosis can promote the transformation from pancreatitis to pancreatic cancer, one of the most lethal malignancies. In the normal pancreas, the acinar component accounts for 82% of the exocrine tissue. Abnormal acinar cells may activate pancreatic stellate cells directly as cellular source of fibrosis or indirectly via releasing various substances and initiate pancreatic fibrosis. A comprehensive understanding of the role of acinar cells in pancreatic fibrosis is critical for designing effective intervention strategies. In this review, we focus on the role of and mechanisms underlying pancreatic acinar injury in pancreatic fibrosis and their potential clinical significance.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 40-53"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9961021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TGF-β mediated drug resistance in solid cancer TGF-β介导的实体癌耐药

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.04.001

Marta Turati , Alexandra Mousset , Nervana Issa , Andrei Turtoi , Roberto Ronca

{"title":"TGF-β mediated drug resistance in solid cancer","authors":"Marta Turati , Alexandra Mousset , Nervana Issa , Andrei Turtoi , Roberto Ronca","doi":"10.1016/j.cytogfr.2023.04.001","DOIUrl":"10.1016/j.cytogfr.2023.04.001","url":null,"abstract":"<div>Transforming growth factor β (TGF-β) is an important signaling molecule which is expressed in three different isoforms in mammals (i.e. TGF-β1, -β2, and -β3). The interaction between TGF-β and its receptor triggers several pathways, which are classified into SMAD-dependent (canonical) and SMAD-independent (non-canonical) signaling, whose activation/transduction is finely regulated by several mechanisms. TGF-β is involved in many physiological and pathological processes, assuming a dualistic role in cancer progression depending on tumor stage. Indeed, TGF-β inhibits cell proliferation in early-stage tumor cells, while it promotes cancer progression and invasion in advanced tumors, where high levels of TGF-β have been reported in both tumor and stromal cells. In particular, TGF-β signaling has been found to be strongly activated in cancers after treatment with chemotherapeutic agents and radiotherapy, resulting in the onset of drug resistance conditions. In this review we provide an up-to-date description of several mechanisms involved in TGF-β-mediated drug resistance, and we report different strategies that are currently under development in order to target TGF-β pathway and increase tumor sensitivity to therapy.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 54-65"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9967058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Brain-derived neurotrophic factor: Its role in energy balance and cancer cachexia 脑源性神经营养因子:在能量平衡和癌症恶病质中的作用

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.07.003

Barış Çerçi , Ayşenur Gök , Aytekin Akyol

{"title":"Brain-derived neurotrophic factor: Its role in energy balance and cancer cachexia","authors":"Barış Çerçi , Ayşenur Gök , Aytekin Akyol","doi":"10.1016/j.cytogfr.2023.07.003","DOIUrl":"10.1016/j.cytogfr.2023.07.003","url":null,"abstract":"<div>Brain-derived neurotrophic factor (BDNF) plays an important role in the development of the central and peripheral nervous system during embryogenesis. In the mature central nervous system, BDNF is required for the maintenance and enhancement of synaptic transmissions and the survival of neurons. Particularly, it is involved in the modulation of neurocircuits that control energy balance through food intake, energy expenditure, and locomotion. Regulation of BDNF in the central nervous system is complex and environmental factors affect its expression in murine models which may reflect to phenotype dramatically. Furthermore, BDNF and its high-affinity receptor tropomyosin receptor kinase B (TrkB), as well as pan-neurotrophin receptor (p75NTR) is expressed in peripheral tissues in adulthood and their signaling is associated with regulation of energy balance. BDNF/TrkB signaling is exploited by cancer cells as well and BDNF expression is increased in tumors. Intriguingly, previously demonstrated roles of BDNF in regulation of food intake, adipose tissue and muscle overlap with derangements observed in cancer cachexia. However, data about the involvement of BDNF in cachectic cancer patients and murine models are scarce and inconclusive. In the future, knock-in and/or knock-out experiments with murine cancer models could be helpful to explore potential new roles for BDNF in the development of cancer cachexia.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 105-116"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10324845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Growth differentiation factor 11: A new hope for the treatment of cardiovascular diseases 生长分化因子11:治疗心血管疾病的新希望

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.007

Yingchun Shao , Yanhong Wang , Jiazhen Xu , Yang Yuan , Dongming Xing

引用次数: 0

Recent progress and prospects for anti-cytokine therapy in preclinical and clinical acute lung injury 抗细胞因子治疗临床前和临床急性肺损伤的研究进展及展望

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.07.002

Guilherme Pasetto Fadanni , João Batista Calixto

{"title":"Recent progress and prospects for anti-cytokine therapy in preclinical and clinical acute lung injury","authors":"Guilherme Pasetto Fadanni , João Batista Calixto","doi":"10.1016/j.cytogfr.2023.07.002","DOIUrl":"10.1016/j.cytogfr.2023.07.002","url":null,"abstract":"<div>Acute respiratory distress syndrome (ARDS) is a heterogeneous cause of respiratory failure that has a rapid onset, a high mortality rate, and for which there is no effective pharmacological treatment. Current evidence supports a critical role of excessive inflammation in ARDS, resulting in several cytokines, cytokine receptors, and proteins within their downstream signalling pathways being putative therapeutic targets. However, unsuccessful trials of anti-inflammatory drugs have thus far hindered progress in the field. In recent years, the prospects of precision medicine and therapeutic targeting of cytokines coevolving into effective treatments have gained notoriety. There is an optimistic and growing understanding of ARDS subphenotypes as well as advances in treatment strategies and clinical trial design. Furthermore, large trials of anti-cytokine drugs in patients with COVID-19 have provided an unprecedented amount of information that could pave the way for therapeutic breakthroughs. While current clinical and nonclinical ARDS research suggest relatively limited potential in monotherapy with anti-cytokine drugs, combination therapy has emerged as an appealing strategy and may provide new perspectives on finding safe and effective treatments. Accurate evaluation of these drugs, however, also relies on well-founded experimental research and the implementation of biomarker-guided stratification in future trials. In this review, we provide an overview of anti-cytokine therapy for acute lung injury and ARDS, highlighting the current preclinical and clinical evidence for targeting the main cytokines individually and the therapeutic prospects for combination therapy.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 13-25"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9974081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

mTOR in programmed cell death and its therapeutic implications mTOR与程序性细胞死亡及其治疗意义

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.002

Yawen Xie, Xianli Lei, Guoyu Zhao, Ran Guo, Na Cui

{"title":"mTOR in programmed cell death and its therapeutic implications","authors":"Yawen Xie, Xianli Lei, Guoyu Zhao, Ran Guo, Na Cui","doi":"10.1016/j.cytogfr.2023.06.002","DOIUrl":"10.1016/j.cytogfr.2023.06.002","url":null,"abstract":"<div>Mechanistic target of rapamycin (mTOR), a highly conserved serine/threonine kinase, is involved in cellular metabolism, protein synthesis, and cell death. Programmed cell death (PCD) assists in eliminating aging, damaged, or neoplastic cells, and is indispensable for sustaining normal growth, fighting pathogenic microorganisms, and maintaining body homeostasis. mTOR has crucial functions in the intricate signaling pathway network of multiple forms of PCD. mTOR can inhibit autophagy, which is part of PCD regulation. Cell survival is affected by mTOR through autophagy to control reactive oxygen species production and the degradation of pertinent proteins. Additionally, mTOR can regulate PCD in an autophagy-independent manner by affecting the expression levels of related genes and phosphorylating proteins. Therefore, mTOR acts through both autophagy-dependent and -independent pathways to regulate PCD. It is conceivable that mTOR exerts bidirectional regulation of PCD, such as ferroptosis, according to the complexity of signaling pathway networks, but the underlying mechanisms have not been fully explained. This review summarizes the recent advances in understanding mTOR-mediated regulatory mechanisms in PCD. Rigorous investigations into PCD-related signaling pathways have provided prospective therapeutic targets that may be clinically beneficial for treating various diseases.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 66-81"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10342677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modulation of IL-33/ST2 signaling as a potential new therapeutic target for cardiovascular diseases 调节IL-33/ST2信号作为心血管疾病潜在的新治疗靶点

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.003

Punniyakoti Veeraveedu Thanikachalam , Srinivasan Ramamurthy , Poojitha Mallapu , Sudhir Rama Varma , Jayaraj Narayanan , Mohammed AS Abourehab , Prashant Kesharwani

{"title":"Modulation of IL-33/ST2 signaling as a potential new therapeutic target for cardiovascular diseases","authors":"Punniyakoti Veeraveedu Thanikachalam , Srinivasan Ramamurthy , Poojitha Mallapu , Sudhir Rama Varma , Jayaraj Narayanan , Mohammed AS Abourehab , Prashant Kesharwani","doi":"10.1016/j.cytogfr.2023.06.003","DOIUrl":"10.1016/j.cytogfr.2023.06.003","url":null,"abstract":"<div>IL-33 belongs to the IL-1 family of cytokines, which function as inducers of Th2 cytokine production by binding with ST2L and IL-1RAcP. This, in turn, activates various signaling pathways, including the mitogen-activated protein kinase (MAPK), the inhibitor of Kappa-B kinase (IKK) pathway, and the phospholipase D-sphingosine kinase pathway. IL-33 has demonstrated protective effects against various cardiovascular diseases (CVDs) by inducing Th2 cytokines and promoting alternative activating M2 polarization. However, the soluble decoy form of ST2 (sST2) mitigates the biological effects of IL-33, exacerbating CVDs. Furthermore, IL-33 also plays a significant role in the development of asthma, arthritis, atopic dermatitis, and anaphylaxis through the activation of Th2 cells and mast cells. In this review, we aim to demonstrate the protective role of IL-33 against CVDs from 2005 to the present and explore the potential of serum soluble ST2 (sST2) as a diagnostic biomarker for CVDs. Therefore, IL-33 holds promise as a potential therapeutic target for the treatment of CVDs.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 94-104"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10024789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Targeting the metabolism and immune system in pancreatic ductal adenocarcinoma: Insights and future directions 针对胰腺导管腺癌的代谢和免疫系统:见解和未来方向

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.006

Dhana Sekhar Reddy Bandi , Sujith Sarvesh , Batoul Farran , Ganji Purnachandra Nagaraju , Bassel F. El-Rayes

{"title":"Targeting the metabolism and immune system in pancreatic ductal adenocarcinoma: Insights and future directions","authors":"Dhana Sekhar Reddy Bandi , Sujith Sarvesh , Batoul Farran , Ganji Purnachandra Nagaraju , Bassel F. El-Rayes","doi":"10.1016/j.cytogfr.2023.06.006","DOIUrl":"10.1016/j.cytogfr.2023.06.006","url":null,"abstract":"<div>Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), presents a challenging landscape due to its complex nature and the highly immunosuppressive tumor microenvironment (TME). This immunosuppression severely limits the effectiveness of immune-based therapies. Studies have revealed the critical role of immunometabolism in shaping the TME and influencing PDAC progression. Genetic alterations, lysosomal dysfunction, gut microbiome dysbiosis, and altered metabolic pathways have been shown to modulate immunometabolism in PDAC. These metabolic alterations can significantly impact immune cell functions, including T-cells, myeloid-derived suppressor cells (MDSCs), and macrophages, evading anti-tumor immunity. Advances in immunotherapy offer promising avenues for overcoming immunosuppressive TME and enhancing patient outcomes. This review highlights the challenges and opportunities for future research in this evolving field. By exploring the connections between immunometabolism, genetic alterations, and the microbiome in PDAC, it is possible to tailor novel approaches capable of improving immunotherapy outcomes and addressing the limitations posed by immunosuppressive TME. Ultimately, these insights may pave the way for improved treatment options and better outcomes for PDAC patients.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 26-39"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10342691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Pathogenic mechanisms of glucocorticoid-induced osteoporosis 糖皮质激素诱发骨质疏松症的发病机制。

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-04-01 DOI: 10.1016/j.cytogfr.2023.03.002

Meng Chen , Wenyu Fu , Huiyun Xu , Chuan-ju Liu

{"title":"Pathogenic mechanisms of glucocorticoid-induced osteoporosis","authors":"Meng Chen , Wenyu Fu , Huiyun Xu , Chuan-ju Liu","doi":"10.1016/j.cytogfr.2023.03.002","DOIUrl":"10.1016/j.cytogfr.2023.03.002","url":null,"abstract":"<div>Glucocorticoid (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including osteoblasts, osteoclasts, and osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the apoptosis of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"70 ","pages":"Pages 54-66"},"PeriodicalIF":13.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10592779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Role of cellular senescence in inflammatory lung diseases 细胞衰老在炎性肺病中的作用

IF 13 2区医学

Cytokine & Growth Factor Reviews Pub Date : 2023-04-01 DOI: 10.1016/j.cytogfr.2023.02.001

Cong Xie , Mai Maititusun Ya Likun , Qing-li Luo , Jing-cheng Dong

{"title":"Role of cellular senescence in inflammatory lung diseases","authors":"Cong Xie , Mai Maititusun Ya Likun , Qing-li Luo , Jing-cheng Dong","doi":"10.1016/j.cytogfr.2023.02.001","DOIUrl":"10.1016/j.cytogfr.2023.02.001","url":null,"abstract":"<div>Cellular senescence, a characteristic sign of aging, classically refers to permanent cell proliferation arrest and is a vital contributor to the pathogenesis of cancer and age-related illnesses. A lot of imperative scientific research has shown that senescent cell aggregation and the release of senescence-associated secretory phenotype (SASP) components can cause lung inflammatory diseases as well. In this study, the most recent scientific progress on cellular senescence and phenotypes was reviewed, including their impact on lung inflammation and the contributions of these findings to understanding the underlying mechanisms and clinical relevance of cell and developmental biology. Within a dozen pro-senescent stimuli, the irreparable DNA damage, oxidative stress, and telomere erosion are all crucial in the long-term accumulation of senescent cells, resulting in sustained inflammatory stress activation in the respiratory system. An emerging role for cellular senescence in inflammatory lung diseases was proposed in this review, followed by the identification of the main ambiguities, thus further understanding this event and the potential to control cellular senescence and pro-inflammatory response activation. In addition, novel therapeutic strategies for the modulation of cellular senescence that might help to attenuate inflammatory lung conditions and improve disease outcomes were also presented in this research.</div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"70 ","pages":"Pages 26-40"},"PeriodicalIF":13.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9942682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4