Molecular and Cellular Endocrinology最新文献_第10页

Dual inhibition of AKT and ERK1/2 pathways restores the expression of progesterone Receptor-B in endometriotic lesions through epigenetic mechanisms 通过表观遗传机制双重抑制 AKT 和 ERK1/2 通路可恢复子宫内膜异位症病灶中孕酮受体-B 的表达

IF 3.8 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-31 DOI: 10.1016/j.mce.2024.112290

Sudipta Dutta , JeHoon Lee , Sakhila K. Banu, Joe A. Arosh

{"title":"Dual inhibition of AKT and ERK1/2 pathways restores the expression of progesterone Receptor-B in endometriotic lesions through epigenetic mechanisms","authors":"Sudipta Dutta , JeHoon Lee , Sakhila K. Banu, Joe A. Arosh","doi":"10.1016/j.mce.2024.112290","DOIUrl":"10.1016/j.mce.2024.112290","url":null,"abstract":"<div><p>Endometriosis is an estrogen-dependent and progesterone-resistant gynecological inflammatory disease of reproductive-age women. Progesterone resistance, loss of progesterone receptor -B (PR-B) in the stromal cells of the endometrium, is one of the hallmarks of endometriosis and a major contributing factor for infertility in endometriosis patients. Loss of PR-B in the stromal cells of the endometriotic lesions poses resistance to the success of progesterone-based therapy. The working hypothesis is that PR-B is hypermethylated and epigenetically silenced, and inhibition of AKT and ERK1/2 pathways will decrease the hypermethylation, reverse the epigenetic silencing, and restore the expression of PR-B via DNA methylation and histone modification mechanisms in the endometriotic lesions. The objectives are to (i) determine the effects of dual inhibition of AKT and ERK1/2 pathways on the expression of PR-B and DNA methylation and histone modification protein machinery in the endometriotic lesions and (ii) identify the underlying epigenetic mechanisms of PR-B restoration in the endometriotic lesions. The results indicate that dual inhibition of AKT and ERK1/2 pathways decreases the hypermethylation, reverses the epigenetic silencing, and restores the expression of PR-B via DNA methylation and H3K9 and H3K27 methylation mechanisms in the endometriotic lesions or endometriotic stromal cells of human origin. These results support the novel concept that restored expression of PR-B in the endometriotic lesions and endometrium may improve the clinical outcome of progesterone therapy in endometriosis patients.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"592 ","pages":"Article 112290"},"PeriodicalIF":3.8,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Legumain-deficient macrophages regulate inflammation and lipid metabolism in adipose tissues to protect against diet-induced obesity 缺失豆豆蛋白酶的巨噬细胞能调节脂肪组织中的炎症和脂质代谢，从而防止饮食引起的肥胖。

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-28 DOI: 10.1016/j.mce.2024.112283

Wanyu Zhang , Shuowen Wang , Zhuo Liu , Ping Qian , Yuanyuan Li , Jianxin Wu

{"title":"Legumain-deficient macrophages regulate inflammation and lipid metabolism in adipose tissues to protect against diet-induced obesity","authors":"Wanyu Zhang , Shuowen Wang , Zhuo Liu , Ping Qian , Yuanyuan Li , Jianxin Wu","doi":"10.1016/j.mce.2024.112283","DOIUrl":"10.1016/j.mce.2024.112283","url":null,"abstract":"<div><p>Adipose tissue macrophages (ATMs) are key players in the development of obesity and associated metabolic inflammation, which contributes to systemic metabolic dysfunction, and understanding the interaction between macrophages and adipocytes is crucial for developing novel macrophage-based strategies against obesity. Here, we found that Legumain (Lgmn), a well-known lysosomal cysteine protease, is expressed mainly in the ATMs of obese mice. To further deﬁne the potential role of Lgmn-expressing macrophages in the generation of an aberrant metabolic state, Lgmn<sup>F/F</sup>; LysM<sup>Cre</sup> mice, which do not express Lgmn in macrophages, were maintained on a high-fat diet (HFD), and metabolic parameters were assessed. Macrophage-specific Lgmn deficiency protects mice against HFD-induced obesity, diminishes the quantity of proinflammatory macrophages in obese adipose tissues, and alleviates hepatic steatosis and insulin resistance. By analysing the transcriptome and proteome of murine visceral white adipose tissue (vWAT) after HFD feeding, we determined that macrophage Lgmn deficiency causes changes in lipid metabolism and the inflammatory response. Furthermore, the reciprocity of macrophage-derived Lgmn with integrin α5β1 in adipocytes was tested via colocalization analyses. It is further demonstrated in macrophage and adipocyte coculture system that macrophage derived Lgmn bound to integrin α5β1 in adipocytes, therefore attenuating PKA activation, downregulating lipolysis-related proteins and eventually exacerbating obesity development. Overall, our study identified Lgmn as a previously unrecognized regulator involved in the interaction between ATMs and adipocytes contributing to diet-induced obesity and suggested that Lgmn is a potential target for treating metabolic disorders.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"592 ","pages":"Article 112283"},"PeriodicalIF":4.1,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141180267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Reduced hepatic AdipoR2 by increased glucocorticoid mediates effect of psychosocial stress to elevate serum cholesterol 糖皮质激素增加导致肝脏 AdipoR2 减少，从而介导了社会心理压力对血清胆固醇升高的影响。

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-28 DOI: 10.1016/j.mce.2024.112282

Qi Wei Guo , Jia Lin , Yi Lin Shen , Yan Jiang Zheng , Xu Chen , Mi Su , Ji Cheng Zhang , Jin Hua Wang , Hui Tang , Guo Ming Su , Zheng Ke Li , Ding Zhi Fang

{"title":"Reduced hepatic AdipoR2 by increased glucocorticoid mediates effect of psychosocial stress to elevate serum cholesterol","authors":"Qi Wei Guo , Jia Lin , Yi Lin Shen , Yan Jiang Zheng , Xu Chen , Mi Su , Ji Cheng Zhang , Jin Hua Wang , Hui Tang , Guo Ming Su , Zheng Ke Li , Ding Zhi Fang","doi":"10.1016/j.mce.2024.112282","DOIUrl":"10.1016/j.mce.2024.112282","url":null,"abstract":"<div><p>Understanding the effects of psychosocial stress on serum cholesterol may offer valuable insights into the relationship between psychological disorders and endocrine diseases. However, these effects and their underlying mechanisms have not been elucidated yet. Here we show that serum corticosterone, total cholesterol and low-density lipoprotein cholesterol (LDL-C) are elevated in a mouse model of psychosocial stress. Furthermore, alterations occur in AdipoR2-mediated AMPK and PPARα signaling pathways in liver, accompanied by a decrease in LDL-C clearance and an increase in cholesterol synthesis. These changes are further verified in wild-type and <em>AdipoR2</em> overexpression HepG2 cells incubated with cortisol and AdipoR agonist, and are finally confirmed by treating wild-type and hepatic-specific <em>AdipoR2</em> overexpression mice with corticosterone. We conclude that increased glucocorticoid mediates the effects of psychosocial stress to elevate serum cholesterol by inhibiting AdipoR2-mediated AMPK and PPARα signaling to decrease LDL-C clearance and increase cholesterol synthesis in liver.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"592 ","pages":"Article 112282"},"PeriodicalIF":4.1,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141180269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Microbial Endocrinology: Host metabolism and appetite hormones interaction with gut microbiome 微生物内分泌学：宿主新陈代谢和食欲激素与肠道微生物组的相互作用。

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-27 DOI: 10.1016/j.mce.2024.112281

Anam Ashraf, Md. Imtaiyaz Hassan

引用次数: 0

Melatonin improves nitric oxide bioavailability in isoproterenol induced myocardial injury 褪黑素可提高一氧化氮在异丙肾上腺素诱导的心肌损伤中的生物利用率

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-24 DOI: 10.1016/j.mce.2024.112279

Ramison Santos , Patrick Turck , Victor de Mello Palma , Fernanda Visioli , Vanessa Duarte Ortiz , Isabel Cristina Teixeira Proença , Tânia Regina G. Fernandes , Elissa Fernandes , Silvio Tasca , Cristina Campos Carraro , Adriane Belló-Klein , Alex Sander da Rosa Araujo , Neelam Khaper , Alexandre Luz de Castro

{"title":"Melatonin improves nitric oxide bioavailability in isoproterenol induced myocardial injury","authors":"Ramison Santos , Patrick Turck , Victor de Mello Palma , Fernanda Visioli , Vanessa Duarte Ortiz , Isabel Cristina Teixeira Proença , Tânia Regina G. Fernandes , Elissa Fernandes , Silvio Tasca , Cristina Campos Carraro , Adriane Belló-Klein , Alex Sander da Rosa Araujo , Neelam Khaper , Alexandre Luz de Castro","doi":"10.1016/j.mce.2024.112279","DOIUrl":"10.1016/j.mce.2024.112279","url":null,"abstract":"<div><p>Isoproterenol administration is associated with cardiac inflammation and decreased NO availability. Melatonin has been reported to have cardioprotective effect. The aim of this study was to investigate the effect of melatonin on NO bioavailability and inflammation in myocardial injury induced by isoproterenol. Isoproterenol was administrated in male Wistar rats for 7 days to induce cardiac injury. The animals were divided into 3 groups: Control, Isoproterenol, Isoproterenol + Melatonin. Animals received melatonin for 7 days. Echocardiographic analysis was performed and the hearts were collected for molecular analysis. Animals that received isoproterenol demonstrated a reduction in left ventricle systolic and diastolic diameter, indicating the presence of concentric hypertrophy. Melatonin was able to attenuate this alteration. Melatonin also improved NO bioavailability and decreased NF-κβ, TNFα and IL-1β expression. In conclusion, melatonin exhibited a cardioprotective effect which was associated with improving NO bioavailability and decreasing the pro-inflammatory proteins.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"591 ","pages":"Article 112279"},"PeriodicalIF":4.1,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141133074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Mesenchymal stem cells improve cardiac function in diabetic rats by reducing cardiac injury biomarkers and downregulating JAK/STAT/iNOS and iNOS/Apoptosis signaling pathways 间充质干细胞通过减少心脏损伤生物标志物和下调 JAK/STAT/iNOS 和 iNOS/Apoptosis 信号通路，改善糖尿病大鼠的心脏功能

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-24 DOI: 10.1016/j.mce.2024.112280

Thoraya Mohamed Elhassan A-Elgadir , Ayed A. Shati , Saif Aboud Alqahtani , Hasnaa A. Ebrahim , Hailah M. Almohaimeed , Asmaa M. ShamsEldeeen , Mohamed A. Haidara , Samaa S. Kamar , Amal F. Dawood , Mahmoud H. El-Bidawy

{"title":"Mesenchymal stem cells improve cardiac function in diabetic rats by reducing cardiac injury biomarkers and downregulating JAK/STAT/iNOS and iNOS/Apoptosis signaling pathways","authors":"Thoraya Mohamed Elhassan A-Elgadir , Ayed A. Shati , Saif Aboud Alqahtani , Hasnaa A. Ebrahim , Hailah M. Almohaimeed , Asmaa M. ShamsEldeeen , Mohamed A. Haidara , Samaa S. Kamar , Amal F. Dawood , Mahmoud H. El-Bidawy","doi":"10.1016/j.mce.2024.112280","DOIUrl":"10.1016/j.mce.2024.112280","url":null,"abstract":"<div><p>Cardiovascular complications are prevalent manifestations of type 2 diabetes mellitus (T2DM) and are usually the main cause of death. This study aims to show the underlying mechanisms of the potential therapeutic effect of mesenchymal stem cells (MSCs) on diabetic cardiac dysfunction. Twenty-four male Wistar rats were randomly assigned to one of three groups The control group received standard laboratory chow, and the groups with T2DM received a single dose of 45 mg/kg body weight of streptozotocin (STZ) after 3 weeks of pretreatment with a high-fat diet (HFD). Eight weeks after the diagnosis of T2DM, rats were divided into two groups: the T2DM model group and the T2DM + MSCs group. BM-MSCs were administered systemically at 2 × 10<sup>6</sup> cells/rat doses.</p><p>A Significant amelioration in Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and dyslipidemia was noted 2 weeks post-administration of MSCs. Administration of MSCs improved dyslipidemia, the altered cardiac injury biomarkers (p ≤ 0.0001), downregulated Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3)/inducible Nitric oxide synthase (iNOS) and iNOS/Apoptosis signaling pathways. This was associated with improved cardiac dysfunction (impaired left ventricular performance and decreased contractility index).</p><p>Our results show that MSCs ameliorate cardiac dysfunction associated with diabetic cardiomyopathy by lowering dyslipidemia and insulin resistance, inhibiting oxidative stress, and inflammation, downregulating JAK2/STAT3/iNOS and iNOS/Apoptosis signaling pathways.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"591 ","pages":"Article 112280"},"PeriodicalIF":4.1,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141131510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

L(1)10Bb serves as a conservative determinant for soma-germline communications via cellular non-autonomous effects within the testicular stem cell niche L(1)10Bb通过睾丸干细胞龛内的细胞非自主效应，成为体细胞与胚系沟通的保守决定因素

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-23 DOI: 10.1016/j.mce.2024.112278

Lei He , Feiteng Sun , Yunhao Wu , Zhiran Li , Yangbo Fu, Qiuru Huang, Jiaxin Li, Zihan Wang, Jiaying Cai, Chenrui Feng, Xiaonan Deng, Han Gu, Xuxin He, Jun Yu, Fei Sun

{"title":"L(1)10Bb serves as a conservative determinant for soma-germline communications via cellular non-autonomous effects within the testicular stem cell niche","authors":"Lei He , Feiteng Sun , Yunhao Wu , Zhiran Li , Yangbo Fu, Qiuru Huang, Jiaxin Li, Zihan Wang, Jiaying Cai, Chenrui Feng, Xiaonan Deng, Han Gu, Xuxin He, Jun Yu, Fei Sun","doi":"10.1016/j.mce.2024.112278","DOIUrl":"https://doi.org/10.1016/j.mce.2024.112278","url":null,"abstract":"<div><p>The testicular stem cell niche is the central regulator of spermatogenesis in <em>Drosophila melanogaster</em>. However, the underlying regulatory mechanisms are unclear. This study demonstrated the crucial role of <em>lethal (1)</em> 10Bb [<em>l(1)</em>10Bb] in regulating the testicular stem cell niche. Dysfunction of <em>l(1)</em>10Bb in early-stage cyst cells led to male fertility disorders and compromised cyst stem cell maintenance. Moreover, the dysfunction of <em>l(1)</em>10Bb in early-stage cyst cells exerted non-autonomous effects on germline stem cell differentiation, independently of hub signals. Notably, our study highlights the rescue of testicular defects through ectopic expression of L(1)10Bb and the human homologous protein BUD31 homolog (BUD31). In addition, <em>l(1)</em>10Bb dysfunction in early-stage cyst cells downregulated the expression of spliceosome subunits in the Sm and the precursor RNA processing complexes. Collectively, our findings established <em>l(1)</em>10Bb as a pivotal factor in the modulation of <em>Drosophila</em> soma-germline communications within the testicular stem cell niche.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"591 ","pages":"Article 112278"},"PeriodicalIF":4.1,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141097483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

TJP1 suppresses trophoblast cell invasion by expressing E2F8 in the human placenta TJP1 通过在人类胎盘中表达 E2F8 抑制滋养层细胞入侵

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-23 DOI: 10.1016/j.mce.2024.112277

Rika Miki , Seiko Matsuo , Takafumi Ushida , Sho Tano , Kenji Imai , Akihiro Nawa , Hiroaki Kajiyama , Tomomi Kotani

{"title":"TJP1 suppresses trophoblast cell invasion by expressing E2F8 in the human placenta","authors":"Rika Miki , Seiko Matsuo , Takafumi Ushida , Sho Tano , Kenji Imai , Akihiro Nawa , Hiroaki Kajiyama , Tomomi Kotani","doi":"10.1016/j.mce.2024.112277","DOIUrl":"https://doi.org/10.1016/j.mce.2024.112277","url":null,"abstract":"<div><p>Adequate extravillous trophoblast (EVT) invasion into the maternal decidua is important for human placental development. We identified that E2F transcription factor 8 (E2F8) suppresses EVT invasion, and that tight junction protein-1 (<em>TJP1</em>) is a potential downstream target gene of E2F8. We investigated the role of TJP1 in the human placenta and regulation of TJP1 expression by E2F8. <em>TJP1</em> expression decreased in <em>E2F8</em> knockdown HTR-8/SVneo cells. TJP1 and E2F8 were co-expressed in villi in the first-trimester placenta and in EVTs and villi in the third-trimester placenta. TJP1 was significantly increased in the pre-eclamptic compared with control placenta. <em>TJP1</em> knockdown increased the invasion of HTR-8/SVneo cells, while TJP1 overexpression inhibited cell invasion. Halo-E2F8 overexpression significantly increased <em>TJP1</em> expression and <em>TJP1</em> transcription compared with control placenta. Our findings suggest that E2F8 promotes <em>TJP1</em> transcription, and that TJP1 expression by E2F8 inhibits EVT invasion. TJP1 and E2F8 may be related to pre-eclampsia pathogenesis.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"591 ","pages":"Article 112277"},"PeriodicalIF":4.1,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141097352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The Guillemin-Yen partnership: A bright light gone dark Guillemin-Yen 合作伙伴关系：黑暗中的曙光

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-22 DOI: 10.1016/j.mce.2024.112276

Eli Y. Adashi MD, MS

引用次数: 0

AMPK inhibits voltage-gated calcium channel-current in rat chromaffin cells AMPK 可抑制大鼠绒毛膜细胞中的电压门控钙通道电流。

IF 4.1 3区医学

Molecular and Cellular Endocrinology Pub Date : 2024-05-20 DOI: 10.1016/j.mce.2024.112275

A.K. Fukumoto-Inukai , K. Bermeo , I. Arenas , M.J. Rosendo-Pineda , J.A. Pimentel-Cabrera , D.E. Garcia

{"title":"AMPK inhibits voltage-gated calcium channel-current in rat chromaffin cells","authors":"A.K. Fukumoto-Inukai , K. Bermeo , I. Arenas , M.J. Rosendo-Pineda , J.A. Pimentel-Cabrera , D.E. Garcia","doi":"10.1016/j.mce.2024.112275","DOIUrl":"10.1016/j.mce.2024.112275","url":null,"abstract":"<div><p>Metabolic changes are critical in the regulation of Ca<sup>2+</sup> influx in central and peripheral neuroendocrine cells. To study the regulation of L-type Ca<sup>2+</sup> channels by AMPK we used biochemical reagents and ATP/glucose-concentration manipulations in rat chromaffin cells. AICAR and Compound-C, at low concentration, significantly induce changes in L-type Ca<sup>2+</sup> channel-current amplitude and voltage dependence. Remarkably, an overlasting decrease in the channel-current density can be induced by lowering the intracellular level of ATP. Accordingly, Ca<sup>2+</sup> channel-current density gradually diminishes by decreasing the extracellular glucose concentration. By using immunofluorescence, a decrease in the expression of Ca<sub>V</sub>1.2 is observed while decreasing extracellular glucose, suggesting that AMPK reduces the number of functional Ca<sup>2+</sup> channels into the plasma membrane. Together, these results support for the first time the dependence of metabolic changes in the maintenance of Ca<sup>2+</sup> channel-current by AMPK. They reveal a key step in Ca<sup>2+</sup> influx in secretory cells.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"591 ","pages":"Article 112275"},"PeriodicalIF":4.1,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141081979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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