Advances in pharmacology最新文献_第9页

Preface. 序言

Advances in pharmacology Pub Date : 2023-01-01 DOI: 10.1016/S1054-3589(23)00031-5

Darryl C Zeldin, John M Seubert

引用次数: 0

Mechanisms of chromate carcinogenesis by chromatin alterations. 染色质改变致铬酸盐癌的机制。

Advances in pharmacology Pub Date : 2023-01-01 DOI: 10.1016/bs.apha.2022.07.001

Hesbon A Zablon, Andrew VonHandorf, Alvaro Puga

{"title":"Mechanisms of chromate carcinogenesis by chromatin alterations.","authors":"Hesbon A Zablon, Andrew VonHandorf, Alvaro Puga","doi":"10.1016/bs.apha.2022.07.001","DOIUrl":"https://doi.org/10.1016/bs.apha.2022.07.001","url":null,"abstract":"In a dynamic environment, organisms must constantly mount an adaptive response to new environmental conditions in order to survive. Novel patterns of gene expression, driven by attendant changes in chromatin architecture, aid in adaptation and survival. Critical mechanisms in the control of gene transcription govern new spatiotemporal chromatin-chromatin interactions that make regulatory DNA elements accessible to the transcription factors that control the response. Consequently, agents that disrupt chromatin structure are likely to have a direct impact on the transcriptional programs of cells and organisms and to drive alterations in fundamental physiological processes. In this regard, hexavalent chromium (Cr(VI)) is of special interest because it interacts directly with cellular proteins, DNA, and other macromolecules, and is likely to upset cell functions that may cause generalized damage to the organism. Here, we will highlight chromium-mediated mechanisms that disrupt chromatin architecture and discuss how these mechanisms are integral to its carcinogenic properties. Emerging evidence indicates that Cr(VI) targets euchromatin, particularly in genomic locations flanking the binding sites of the essential transcription factors CTCF and AP1, and, in so doing, they disrupt nucleosomal architecture. Ultimately, the ensuing changes, if occurring in critical regulatory domains, may establish a new chromatin state, either toxic or adaptive, that will be governed by the corresponding gene transcription changes in key biological processes associated with that state.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"96 ","pages":"1-23"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10869505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Breast carcinogenesis induced by organophosphorous pesticides. 有机磷农药致乳腺癌的研究。

Advances in pharmacology Pub Date : 2023-01-01 DOI: 10.1016/bs.apha.2022.10.003

Gloria M Calaf

{"title":"Breast carcinogenesis induced by organophosphorous pesticides.","authors":"Gloria M Calaf","doi":"10.1016/bs.apha.2022.10.003","DOIUrl":"https://doi.org/10.1016/bs.apha.2022.10.003","url":null,"abstract":"Breast cancer is a major health threat to women worldwide and the leading cause of cancer-related death. The use of organophosphorous pesticides has increased in agricultural environments and urban settings, and there is evidence that estrogen may increase breast cancer risk in women. The mammary gland is an excellent model for examining its susceptibility to different carcinogenic agents due to its high cell proliferation capabilities associated with the topography of the mammary parenchyma and specific stages of gland development. Several experimental cellular models are presented here, in which the animals were exposed to chemical compounds such as pesticides, and endogenous substances such as estrogens that exert a significant effect on normal breast cell processes at different levels. Such models were developed by the effect of malathion, parathion, and eserine, influenced by estrogen demonstrating features of cancer initiation in vivo as tumor formation in rodents; and in vitro in the immortalized normal breast cell line MCF-10F, that when transformed showed signs of carcinogenesis such as increased cell proliferation, anchorage independence, invasive capabilities, modulation of receptors and genomic instability. The role of acetylcholine was also demonstrated in the MCF-10F, suggesting a role not only as a neurotransmitter but also with other functions, such as induction of cell proliferation, playing an important role in cancer. Of note, this is a unique experimental approach that identifies mechanistic signs that link organophosphorous pesticides with breast carcinogenesis.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"96 ","pages":"71-117"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9076116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Genomic and non-genomic effects of glucocorticoids in respiratory diseases. 糖皮质激素在呼吸系统疾病中的基因组和非基因组效应。

Advances in pharmacology Pub Date : 2023-01-01 DOI: 10.1016/bs.apha.2023.04.006

Zhao-Yong Lee, Thai Tran

引用次数: 0

20-Hydroxyeicosatetraenoic acid (20-HETE): Bioactions, receptors, vascular function, cardiometabolic disease and beyond. 20-羟基二碳四烯酸(20-HETE):生物作用、受体、血管功能、心脏代谢疾病及其他。

Advances in pharmacology Pub Date : 2023-01-01 Epub Date: 2023-02-24 DOI: 10.1016/bs.apha.2023.01.002

Jonathan V Pascale, Alexandra Wolf, Yonaton Kadish, Danielle Diegisser, Melissa-Maria Kulaprathazhe, Danait Yemane, Samir Ali, Namhee Kim, David E Baruch, Muhamad Afiq Faisal Yahaya, Ercument Dirice, Adeniyi M Adebesin, John R Falck, Michal L Schwartzman, Victor Garcia

{"title":"20-Hydroxyeicosatetraenoic acid (20-HETE): Bioactions, receptors, vascular function, cardiometabolic disease and beyond.","authors":"Jonathan V Pascale, Alexandra Wolf, Yonaton Kadish, Danielle Diegisser, Melissa-Maria Kulaprathazhe, Danait Yemane, Samir Ali, Namhee Kim, David E Baruch, Muhamad Afiq Faisal Yahaya, Ercument Dirice, Adeniyi M Adebesin, John R Falck, Michal L Schwartzman, Victor Garcia","doi":"10.1016/bs.apha.2023.01.002","DOIUrl":"10.1016/bs.apha.2023.01.002","url":null,"abstract":"Vascular function is dynamically regulated and dependent on a bevy of cell types and factors that work in concert across the vasculature. The vasoactive eicosanoid, 20-Hydroxyeicosatetraenoic acid (20-HETE) is a key player in this system influencing the sensitivity of the vasculature to constrictor stimuli, regulating endothelial function, and influencing the renin angiotensin system (RAS), as well as being a driver of vascular remodeling independent of blood pressure elevations. Several of these bioactions are accomplished through the ligand-receptor pairing between 20-HETE and its high-affinity receptor, GPR75. This 20-HETE axis is at the root of various vascular pathologies and processes including ischemia induced angiogenesis, arteriogenesis, septic shock, hypertension, atherosclerosis, myocardial infarction and cardiometabolic diseases including diabetes and insulin resistance. Pharmacologically, several preclinical tools have been developed to disrupt the 20-HETE axis including 20-HETE synthesis inhibitors (DDMS and HET0016), synthetic 20-HETE agonist analogues (20-5,14-HEDE and 20-5,14-HEDGE) and 20-HETE receptor blockers (AAA and 20-SOLA). Systemic or cell-specific therapeutic targeting of the 20-HETE-GPR75 axis continues to be an invaluable approach as studies examine the molecular underpinnings activated by 20-HETE under various physiological settings. In particular, the development and characterization of 20-HETE receptor blockers look to be a promising new class of compounds that can provide a considerable benefit to patients suffering from these cardiovascular pathologies.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"97 ","pages":"229-255"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10683332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10020329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Insights into the role of the resolvin D2-GPR18 signaling axis in cardiovascular physiology and disease. 解析蛋白D2-GPR18信号轴在心血管生理和疾病中的作用

Advances in pharmacology Pub Date : 2023-01-01 DOI: 10.1016/bs.apha.2022.12.005

Matthew Spite, Gabrielle Fredman

引用次数: 0

Progress in the development of kinase inhibitors for treating asthma and COPD. 激酶抑制剂治疗哮喘和慢性阻塞性肺病的研究进展。

Advances in pharmacology Pub Date : 2023-01-01 Epub Date: 2023-05-03 DOI: 10.1016/bs.apha.2023.04.004

Nathaniel McClean, Jeffery D Hasday, Paul Shapiro

{"title":"Progress in the development of kinase inhibitors for treating asthma and COPD.","authors":"Nathaniel McClean, Jeffery D Hasday, Paul Shapiro","doi":"10.1016/bs.apha.2023.04.004","DOIUrl":"10.1016/bs.apha.2023.04.004","url":null,"abstract":"Current therapies to mitigate inflammatory responses involved in airway remodeling and associated pathological features of asthma and chronic obstructive pulmonary disease (COPD) are limited and largely ineffective. Inflammation and the release of cytokines and growth factors activate kinase signaling pathways that mediate changes in airway mesenchymal cells such as airway smooth muscle cells and lung fibroblasts. Proliferative and secretory changes in mesenchymal cells exacerbate the inflammatory response and promote airway remodeling, which is often characterized by increased airway smooth muscle mass, airway hyperreactivity, increased mucus secretion, and lung fibrosis. Thus, inhibition of relevant kinases has been viewed as a potential therapeutic approach to mitigate the debilitating and, thus far, irreversible airway remodeling that occurs in asthma and COPD. Despite FDA approval of several kinase inhibitors for the treatment of proliferative disorders, such as cancer and inflammation associated with rheumatoid arthritis and ulcerative colitis, none of these drugs have been approved to treat asthma or COPD. This review will provide a brief overview of the role kinases play in the pathology of asthma and COPD and an update on the status of kinase inhibitors currently in clinical trials for the treatment of obstructive pulmonary disease. In addition, potential issues associated with the current kinase inhibitors, which have limited their success as therapeutic agents in treating asthma or COPD, and alternative approaches to target kinase functions will be discussed.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"98 ","pages":"145-178"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9908284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis. 铬致癌作用的表观遗传学和表转录组学机制。

Advances in pharmacology Pub Date : 2023-01-01 Epub Date: 2022-08-26 DOI: 10.1016/bs.apha.2022.07.002

Zhishan Wang, Chengfeng Yang

{"title":"Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.","authors":"Zhishan Wang, Chengfeng Yang","doi":"10.1016/bs.apha.2022.07.002","DOIUrl":"10.1016/bs.apha.2022.07.002","url":null,"abstract":"Hexavalent chromium [Cr(VI)], a Group I carcinogen classified by the International Agency for Research on Cancer (IARC), represents one of the most common occupational and environmental pollutants. The findings from human epidemiological and laboratory animal studies show that long-term exposure to Cr(VI) causes lung cancer and other cancer. Although Cr(VI) is a well-recognized carcinogen, the mechanism of Cr(VI) carcinogenesis has not been well understood. Due to the fact that Cr(VI) undergoes a series of metabolic reductions once entering cells to generate reactive Cr metabolites and reactive oxygen species (ROS) causing genotoxicity, Cr(VI) is generally considered as a genotoxic carcinogen. However, more and more studies have demonstrated that acute or chronic Cr(VI) exposure also causes epigenetic dysregulations including changing DNA methylation, histone posttranslational modifications and regulatory non-coding RNA (microRNA and long non-coding RNA) expressions. Moreover, emerging evidence shows that Cr(VI) exposure is also capable of altering cellular epitranscriptome. Given the increasingly recognized importance of epigenetic and epitranscriptomic dysregulations in cancer initiation and progression, it is believed that Cr(VI) exposure-caused epigenetic and epitranscriptomic changes could play important roles in Cr(VI) carcinogenesis. The goal of this chapter is to review the epigenetic and epitranscriptomic effects of Cr(VI) exposure and discuss their roles in Cr(VI) carcinogenesis. Better understanding the mechanism of Cr(VI) carcinogenesis may identify new molecular targets for more efficient prevention and treatment of cancer resulting from Cr(VI) exposure.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"96 ","pages":"241-265"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10565670/pdf/nihms-1921925.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9913040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Tungsten toxicity and carcinogenesis. 钨的毒性和致癌作用。

Advances in pharmacology Pub Date : 2023-01-01 Epub Date: 2022-12-20 DOI: 10.1016/bs.apha.2022.10.004

Alicia M Bolt

{"title":"Tungsten toxicity and carcinogenesis.","authors":"Alicia M Bolt","doi":"10.1016/bs.apha.2022.10.004","DOIUrl":"10.1016/bs.apha.2022.10.004","url":null,"abstract":"Tungsten is an emerging contaminant in the environment. Research has demonstrated that humans are exposed to high levels of tungsten in certain settings, primarily due to increased use of tungsten in industrial applications. However, our understanding of the potential human health risks of tungsten exposure is still limited. An important point we have learned about the toxicity profile of tungsten is that it is complex because tungsten can often augment the effects of other co-exposures or co-stressors, which could result in greater toxicity or more severe disease. This has shaped the tungsten toxicology field and the types of research questions being investigated. This has particularly been true when evaluating the toxicity profile of tungsten metal alloys in combination with cobalt. In this chapter, the current state of the tungsten toxicology field will be discussed focusing on data investigating tungsten carcinogenicity and other major toxicities including pulmonary, cardiometabolic, bone, and immune endpoints, either alone or in combination with other metals. Environmental and human monitoring data will also be discussed to highlight human populations most at risk of exposure to high concentrations of tungsten, the forms of tungsten present in each setting, and exposure levels in each population.","PeriodicalId":7366,"journal":{"name":"Advances in pharmacology","volume":"96 ","pages":"119-150"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11003356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9076112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miRNAs and arsenic-induced carcinogenesis. miRNA 与砷诱发的癌变。

Advances in pharmacology Pub Date : 2023-01-01 Epub Date: 2023-02-06 DOI: 10.1016/bs.apha.2022.10.002

Alexandra N Nail, Ana P Ferragut Cardoso, Lakyn K Montero, J Christopher States

引用次数: 0