生理学报 Pub Date : 2024-12-25

Yi-Bing Ke, Dawuti Abudoukeremu, Hao-Ran Guo, Yong-Ping Wang

{"title":"[Research progress on molecular mechanism related to skeletal muscle atrophy].","authors":"Yi-Bing Ke, Dawuti Abudoukeremu, Hao-Ran Guo, Yong-Ping Wang","doi":"","DOIUrl":"","url":null,"abstract":"The maintenance of skeletal muscle quality involves various signal pathways that interact with each other. Under normal physiological conditions, these intersecting signal pathways regulate and coordinate the hypertrophy and atrophy of skeletal muscles, balancing the protein synthesis and degradation of muscle. When the total rate of protein synthesis exceeds that of protein degradation, the muscle gradually becomes enlarged, while when the total rate of protein synthesis is lower than that of protein degradation, the muscle shrinks. Myocyte atrophy mainly involves two protein degradation pathways, namely ubiquitin-proteasome and autophagy-lysosome. Protein degradation pathway is activated during muscle atrophy, resulting in the loss of muscle mass. Muscle atrophy can occur under various conditions such as malnutrition, aging and cachexia. Skeletal muscle atrophy caused by orthopedic diseases mainly includes disuse muscular atrophy caused by fracture and denervation muscular atrophy. The signal pathways that control and coordinate protein synthesis and degradation in skeletal muscle include insulin-like growth factor 1 (IGF1)-Akt-mammalian target of rapamycin (mTOR), myostatin-activin A-Smad, G protein α inhibitory peptide 2 (Gαi2)-PKC, nuclear factor κB (NF-κB), ectodysplasin A2 receptor (EDA2R)-NF-κB inducing kinase (NIK) and mitogen-activated protein kinase (MAPK) pathways. This paper provides a comprehensive review of the protein degradation pathways in skeletal muscle atrophy and the associated signal pathways regulating protein degradation in muscular atrophy.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 6","pages":"1056-1068"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942527","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

[Revisiting the vasopressin V2 receptor]. [重新审视抗利尿激素V2受体]。

生理学报 Pub Date : 2024-12-25

Meng Li, Wei-Dong Wang, Chun-Ling Li

引用次数: 0

[NMDA receptors in prelimbic cortex neurons projecting to paraventricular nucleus of the thalamus are associated with morphine withdrawal memory retrieval]. [投射到丘脑室旁核的边缘皮层前神经元中的NMDA受体与吗啡戒断记忆恢复有关]。

生理学报 Pub Date : 2024-12-25

Chen-Shan Chu, Ya-Xian Wen, Qian-Ru Shen, Bin Lai, Ming Chen, Ping Zheng

{"title":"[NMDA receptors in prelimbic cortex neurons projecting to paraventricular nucleus of the thalamus are associated with morphine withdrawal memory retrieval].","authors":"Chen-Shan Chu, Ya-Xian Wen, Qian-Ru Shen, Bin Lai, Ming Chen, Ping Zheng","doi":"","DOIUrl":"","url":null,"abstract":"At present, the problem of drug addiction treatment mainly lies in the high relapse rate of drug addicts. Addictive drugs will bring users a strong sense of euphoria and promote drug seeking. Once the drug is withdrawn, there will be withdrawal symptoms such as strong negative emotions and uncomfortable physical reactions. The recurrence of context-induced withdrawal memory is an important reason for drug relapse. Our previous study has shown increased c-Fos expression in prelimbic cortex (PrL) neurons projecting to paraventricular nucleus of the thalamus (PVT) (PrL-PVT) during conditioned context-induced retrieval of morphine withdrawal memory. However, whether PrL-PVT neurons are involved in withdrawal memory retrieval and the underlying molecular mechanisms remain unknown. In this study, we used conditioned place aversion (CPA) model combined with in vivo calcium signal recording, chemogenetics and nucleus drug injection methods to investigate the role and molecular mechanism of PrL-PVT neurons in retrieval of morphine withdrawal memory. The results showed that the calcium signals of PrL-PVT neurons were significantly enhanced by withdrawal-related context; Inhibition of PrL-PVT neurons blocked the conditioned context-induced morphine withdrawal memory retrieval; Activation of PrL-PVT neurons caused animals to escape from the context; After the inhibition of NMDA receptors in the PrL, withdrawal-related context failed to increase c-Fos and Arc expressions in PrL-PVT neurons. The above results suggest that NMDA receptors in PrL-PVT neurons are associated with retrieval of morphine withdrawal memory. This study is of great significance for further understanding the neural circuit mechanism of withdrawal memory retrieval as well as the intervention and prevention of drug relapse.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 6","pages":"917-926"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942512","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

[Research advances on the structure, function, and related diseases of TREK-1 potassium channels]. 【TREK-1钾通道的结构、功能及相关疾病研究进展】。

生理学报 Pub Date : 2024-12-25

Xiao-Ling Li, Yang Li, Hong Zhang

引用次数: 0

[Progress on the role of N-end rule pathways in protein degradation]. [n端规则通路在蛋白质降解中的作用研究进展]。

生理学报 Pub Date : 2024-12-25

Na-Xin Xu, Yong Liu, Yi Wang, Shu-Kuan Ling

{"title":"[Progress on the role of N-end rule pathways in protein degradation].","authors":"Na-Xin Xu, Yong Liu, Yi Wang, Shu-Kuan Ling","doi":"","DOIUrl":"","url":null,"abstract":"The N-end rule pathway is a protein degradation pathway mediated by the ubiquitin-proteasome system, which specifically targets and degrades target proteins by recognizing specific residues at the N-terminus of the proteins. The residues which play a crucial role in the N-end rule pathway are called degrons, also known as N-degrons, as they are usually unstable at the N-terminal end of the protein. Currently, several N-end rule pathways have been identified in the eukaryotes, including the Arg/N-end rule, Ac/N-end rule, and Pro/N-end rule pathways, as well as the recently discovered Gly/N-end rule pathway. The Ac/N-end rule pathway targets proteins containing N-terminal acetylation (Nt-acetylation) residues. The Arg/N-end rule pathway, on the other hand, targets certain unacetylated residues and involves N-terminal arginylation. For proteins with N-terminal proline (Pro) and glycine (Gly) residues, they are neither modified by acetylation nor recognized through the Arg/N-end rule pathway. Therefore, these proteins are primarily recognized and degraded through the Pro/N-end rule pathway and the Gly/N-end rule pathway. The regulation of specific proteins through N-end rule pathway-mediated degradation plays an important role in numerous physiological and pathological processes, such as cardiovascular development, neurogenesis, meiosis, spermatogenesis, HPV infection, and cell apoptosis. In this review, we summarize the role and mechanisms of several known N-end rule pathways and discuss their relationship with certain diseases. As an independent protein degradation system, the N-end rule pathways still hold countless biological secrets waiting for exploring. The comprehensive understanding of these pathways could potentially uncover novel therapeutic targets for various diseases.","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 6","pages":"987-1000"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942515","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

[Cardiac β-adrenergic receptor regulation of mitochondrial function in heart failure]. [心脏β-肾上腺素能受体对心力衰竭线粒体功能的调节]。

生理学报 Pub Date : 2024-12-25

Ai-Ming Liu, Wen-Li Xu, Han Xiao, Er-Dan Dong

引用次数: 0

[Research progress on anti-aging effects of β-nicotinamide mononucleotide (NMN)]. [β-烟酰胺单核苷酸（NMN）抗衰老作用研究进展]。

生理学报 Pub Date : 2024-12-25

Miao Han, Jin-Lian Hua

引用次数: 0

The landscape of GPCR in the skin epidermal stem cells: From the basic to the clinical. GPCR在皮肤表皮干细胞中的应用前景：从基础到临床。

生理学报 Pub Date : 2024-12-25

Zhi-Lin Zhang, Xiao-Qing Ma, Zhao-Tian Zhang, Rong-Hao Zhang, Ru-Tao Cui