In eukaryotes, autophagy helps maintain cellular homeostasis by degrading and recycling cytoplasmic materials via a tightly regulated pathway.Over the past few decades, significant progress has been made towards under...In eukaryotes, autophagy helps maintain cellular homeostasis by degrading and recycling cytoplasmic materials via a tightly regulated pathway.Over the past few decades, significant progress has been made towards understanding the physiological functions and molecular regulation of autophagy in plant cells. Increasing evidence indicates that autophagy is essential for plant responses to several developmental and environmental cues, functioning in diverse processes such as senescence, male fertility, root meristem maintenance, responses to nutrient starvation,and biotic and abiotic stress. Recent studies have demonstrated that, similar to nonplant systems,the modulation of core proteins in the plant autophagy machinery by posttranslational modifications such as phosphorylation, ubiquitination,lipidation, S-sulfhydration, S-nitrosylation, and acetylation is widely involved in the initiation and progression of autophagy. Here, we provide an overview of the physiological roles and posttranslational regulation of autophagy in plants.展开更多
With the ever increasing application of electronic technology, our exposure to artificial electromagnetic energy is also rapidly increasing. Electromagnetic radiation （EMR） is the fourth largest source of pollution,...With the ever increasing application of electronic technology, our exposure to artificial electromagnetic energy is also rapidly increasing. Electromagnetic radiation （EMR） is the fourth largest source of pollution, after air, water, and noise.展开更多
The global increase in lifespan noted not only in developed nations,but also in large developing countries parallels an observed increase in a significant number of noncommunicable diseases,most notable neurodegenerat...The global increase in lifespan noted not only in developed nations,but also in large developing countries parallels an observed increase in a significant number of noncommunicable diseases,most notable neurodegenerative disorders.Neurodegenerative disorders present a number of challenges for treatment options that do not resolve disease progression.Furthermore,it is believed by the year 2030,the services required to treat cognitive disorders in the United States alone will exceed$2 trillion annually.Mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae),the mechanistic target of rapamycin,and the pathways of autophagy and apoptosis offer exciting avenues to address these challenges by focusing upon core cellular mechanisms that may significantly impact nervous system disease.These pathways are intimately linked such as through cell signaling pathways involving protein kinase B and can foster,sometimes in conjunction with trophic factors,enhanced neuronal survival,reduction in toxic intracellular accumulations,and mitochondrial stability.Feedback mechanisms among these pathways also exist that can oversee reparative processes in the nervous system.However,mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1,mechanistic target of rapamycin,and autophagy can lead to cellular demise under some scenarios that may be dependent upon the precise cellular environment,warranting future studies to effectively translate these core pathways into successful clinical treatment strategies for neurodegenerative disorders.展开更多
[目的]明确痰瘀同治方对心肌缺血区和动脉粥样硬化(atherosclerosis,AS)斑块内血管新生的双向调节作用,探讨自噬在其中的调控机制。[方法]选取载脂蛋白E基因敲除(Apolipoprotein E gene knockout,ApoE-/-)小鼠20只,随机分为模型对照组...[目的]明确痰瘀同治方对心肌缺血区和动脉粥样硬化(atherosclerosis,AS)斑块内血管新生的双向调节作用,探讨自噬在其中的调控机制。[方法]选取载脂蛋白E基因敲除(Apolipoprotein E gene knockout,ApoE-/-)小鼠20只,随机分为模型对照组和痰瘀同治(Tanyu Tongzhi,TYTZ)组,每组10只,饲喂高脂饲料;另取C57BL/6J小鼠10只为正常对照组,饲喂基础饲料。饲喂4周后,模型对照组和TYTZ组皮下注射异丙肾上腺素针100mg/kg,连续2d,正常对照组皮下注射等量0.9%氯化钠注射液。造模成功后4周,TYTZ组给予TYTZ方流浸膏2145mg/(kg·d),以蒸馏水稀释成0.4mL灌胃,模型对照组和正常对照组给予等量蒸馏水灌胃。给药6周后,用CD31免疫组化染色观察心肌缺血区和主动脉的新生血管密度。Western blot检测心肌组织和主动脉微管相关蛋白1轻链3(microtubule-associated protein 1 light chain 3,LC3)Ⅱ/Ⅰ蛋白表达。[结果]免疫组化染色结果显示,模型对照组心肌组织和主动脉组织CD31表达均显著高于正常对照组(P<0.05);TYTZ组心肌组织CD31表达明显高于模型对照组(P<0.05),而主动脉组织CD31表达则明显低于模型对照组(P<0.05)。Western blot结果显示,模型对照组心肌组织和主动脉组织LC3Ⅱ/Ⅰ蛋白表达水平均明显高于正常对照组(P<0.05);TYTZ组心肌组织LC3Ⅱ/Ⅰ蛋白表达水平显著高于模型对照组(P<0.05),而主动脉组织LC3Ⅱ/Ⅰ蛋白表达则明显低于模型对照组(P<0.05)。[结论]TYTZ方在抑制AS斑块内血管新生的同时能够促进心肌缺血区的血管新生,该方对自噬水平的双向调节作用可能是其中的调控机制。展开更多
基金supported by the National Natural Science Foundation of China (Projects 31725004 and 31670276 to S.X.and Project 31800217 to H.Q.)the Natural Science Foundation of Guangdong Province,China (Project 2017A030308008to S.X. and Project 2018A030313210 to H.Q.)Sun Yat-sen University (Project 19lgpy202 to H.Q.)。
文摘In eukaryotes, autophagy helps maintain cellular homeostasis by degrading and recycling cytoplasmic materials via a tightly regulated pathway.Over the past few decades, significant progress has been made towards understanding the physiological functions and molecular regulation of autophagy in plant cells. Increasing evidence indicates that autophagy is essential for plant responses to several developmental and environmental cues, functioning in diverse processes such as senescence, male fertility, root meristem maintenance, responses to nutrient starvation,and biotic and abiotic stress. Recent studies have demonstrated that, similar to nonplant systems,the modulation of core proteins in the plant autophagy machinery by posttranslational modifications such as phosphorylation, ubiquitination,lipidation, S-sulfhydration, S-nitrosylation, and acetylation is widely involved in the initiation and progression of autophagy. Here, we provide an overview of the physiological roles and posttranslational regulation of autophagy in plants.
基金supported by the National Natural Science Foundation of China[No.31570847]
文摘With the ever increasing application of electronic technology, our exposure to artificial electromagnetic energy is also rapidly increasing. Electromagnetic radiation （EMR） is the fourth largest source of pollution, after air, water, and noise.
基金supported by American Diabetes AssociationAmerican Heart Association+3 种基金National Institutes of Health-National Institute of Environmental Health SciencesNational Institutes of Health-National Institute on AgingNational Institutes of Health-National Institute of Neurological DisordersNational Institutes of Health-American Recovery and Reinvestment(to KM)。
文摘The global increase in lifespan noted not only in developed nations,but also in large developing countries parallels an observed increase in a significant number of noncommunicable diseases,most notable neurodegenerative disorders.Neurodegenerative disorders present a number of challenges for treatment options that do not resolve disease progression.Furthermore,it is believed by the year 2030,the services required to treat cognitive disorders in the United States alone will exceed$2 trillion annually.Mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae),the mechanistic target of rapamycin,and the pathways of autophagy and apoptosis offer exciting avenues to address these challenges by focusing upon core cellular mechanisms that may significantly impact nervous system disease.These pathways are intimately linked such as through cell signaling pathways involving protein kinase B and can foster,sometimes in conjunction with trophic factors,enhanced neuronal survival,reduction in toxic intracellular accumulations,and mitochondrial stability.Feedback mechanisms among these pathways also exist that can oversee reparative processes in the nervous system.However,mammalian forkhead transcription factors,silent mating type information regulation 2 homolog 1,mechanistic target of rapamycin,and autophagy can lead to cellular demise under some scenarios that may be dependent upon the precise cellular environment,warranting future studies to effectively translate these core pathways into successful clinical treatment strategies for neurodegenerative disorders.
