Cell Biochemistry and Function最新文献_第7页

What Can Really Be Considered a Syndrome? An Insight Based on 16p11.2 Microduplication 什么才能真正被视为综合征？基于 16p11.2 微重复的见解

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-12 DOI: 10.1002/cbf.4121

Rafaella Mergener, Lívia Polisseni Cotta Nascimento, Ana Kalise Böttcher, Marcela Rodrigues Nunes, Paulo Ricardo Gazzola Zen

引用次数: 0

Research Progress on the Role of Cartilage Endplate in Intervertebral Disc Degeneration 软骨终板在椎间盘退变中的作用研究进展

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-12 DOI: 10.1002/cbf.4118

Zhong Ma, Xin Liu, Mingtao Zhang, Zuolong Wu, Xianxu Zhang, Shicheng Li, Jiangdong An, Zhiqiang Luo

{"title":"Research Progress on the Role of Cartilage Endplate in Intervertebral Disc Degeneration","authors":"Zhong Ma, Xin Liu, Mingtao Zhang, Zuolong Wu, Xianxu Zhang, Shicheng Li, Jiangdong An, Zhiqiang Luo","doi":"10.1002/cbf.4118","DOIUrl":"https://doi.org/10.1002/cbf.4118","url":null,"abstract":"<div>\u0000 \u0000 <p>Low back pain significantly impacts individuals' quality of life, with intervertebral disc degeneration (IDD) being a primary contributor to this condition. Currently, IDD treatment primarily focuses on symptom management and does not achieve a definitive cure. The cartilage endplate (CEP), a crucial nutrient-supplying tissue of the intervertebral disc, plays a pivotal role in disc degeneration. This review examines the mechanisms underlying CEP degeneration, summarizing recent advancements in understanding the structure and function of CEP, the involvement of various signaling pathways, and the roles of cartilage endplate stem cells (CESCs) and exosomes (Exos) in this process. The aim of this review is to provide a comprehensive reference for future research on CEP. Despite progress in understanding the role of CEP in IDD, the mechanisms underlying CEP degeneration remain incompletely elucidated. Future research poses significant challenges, necessitating further investigations to elucidate the complexities of CEP.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Panax notoginseng Saponins Ameliorate Gamma Radiation-Mediated Damages in Human Peripheral Blood Monocytes and Swiss Albino Mice 三七皂苷能减轻伽马辐射对人类外周血单核细胞和瑞士白化小鼠造成的损伤

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-12 DOI: 10.1002/cbf.4115

Ming-Yu Yang, Xing-Hua Zhao

{"title":"Panax notoginseng Saponins Ameliorate Gamma Radiation-Mediated Damages in Human Peripheral Blood Monocytes and Swiss Albino Mice","authors":"Ming-Yu Yang, Xing-Hua Zhao","doi":"10.1002/cbf.4115","DOIUrl":"https://doi.org/10.1002/cbf.4115","url":null,"abstract":"<div>\u0000 \u0000 <p>In this study, the protective effects of <i>Panax notoginseng</i> saponins (PNS) against gamma radiation-induced DNA damage and associated physiological alterations in Swiss albino mice were investigated. Exposure to gamma radiation led to a dose-dependent increase in cytokinesis-blocked micronuclei (CBMN) double-strand DNA breaks (DSBs), dicentric aberrations (DC), formation in peripheral blood mononuclear cells. However, pretreatment with PNS at concentrations of 1, 5, and 10 µg/mL significantly attenuated the frequencies of DC and CBMN in a concentration-dependent manner. PNS administration before radiation exposure also reduced radiation-induced DSBs in BL, indicating protection against reactive oxygen species generation and DNA damage. Notably, pretreatment with PNS at 10 µg/mL prevented the overexpression of γ-H2AX, proteins associated with DNA damage response, in irradiated mice. In addition, in vivo studies showed intraperitoneal administration of PNS (25 mg/kg body weight) for 1 h before radiation exposure mitigated lipid peroxidation levels and restored antioxidant status, countering oxidative damage induced by gamma radiation. Furthermore, PNS pretreatment reversed the decrease in hemoglobin (Hb) content, white blood cell count, and red blood cell count in irradiated mice, indicating preservation of hematological parameters. Overall, PNS demonstrated an anticlastogenic effect by modulating radiation-induced DSBs and preventing oxidative damage, thus highlighting its potential as a protective agent against radiation-induced DNA damage and associated physiological alterations. Clinically, PNS will be beneficial for cancer patients undergoing radiotherapy, but their pharmacological properties and toxicity profiles need to be studied.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulatory Mechanism of Autophagy in Premature Ovarian Failure 自噬对卵巢早衰的调控机制

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-10 DOI: 10.1002/cbf.4122

Ziwen Ding, Genbao Shao, Mingyang Li

引用次数: 0

Curcumin Prevents Renal Damage of l-NAME Induced Hypertension in by Reducing MMP-2 and MMP-9 姜黄素通过减少 MMP-2 和 MMP-9 防止 l-NAME 诱导的高血压对肾脏的损伤

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-08 DOI: 10.1002/cbf.4119

Bruna Pinheiro Pereira, Alessandra Oliveira Silva, Wanessa Mayumi Carvalho Awata, Gustavo Félix Pimenta, Jéssyca Milene Ribeiro, Carolina Aparecida de Faria Almeida, Carla Renata Kitanishi Antonietto, Luis Felipe Cunha dos Reis, Alessandra Esteves, Larissa Helena Lobo Torres, Fernanda Borges de Araújo Paula, Sílvia Graciela Ruginsk, Carlos Renato Tirapelli, Ellen Rizzi, Carla Speroni Ceron

{"title":"Curcumin Prevents Renal Damage of l-NAME Induced Hypertension in by Reducing MMP-2 and MMP-9","authors":"Bruna Pinheiro Pereira, Alessandra Oliveira Silva, Wanessa Mayumi Carvalho Awata, Gustavo Félix Pimenta, Jéssyca Milene Ribeiro, Carolina Aparecida de Faria Almeida, Carla Renata Kitanishi Antonietto, Luis Felipe Cunha dos Reis, Alessandra Esteves, Larissa Helena Lobo Torres, Fernanda Borges de Araújo Paula, Sílvia Graciela Ruginsk, Carlos Renato Tirapelli, Ellen Rizzi, Carla Speroni Ceron","doi":"10.1002/cbf.4119","DOIUrl":"10.1002/cbf.4119","url":null,"abstract":"<div>\u0000 \u0000 <p>In the present study, we investigated whether curcumin administration would interfere with the main renal features of <span>l</span>-NAME-induced hypertension model. For this purpose, we conducted both in vitro and in vivo experiments to evaluate renal indicators of inflammation, oxidative stress, and metalloproteinases (MMPs) expression/activity. Hypertension was induced by <span>l</span>-NAME (70 mg/kg/day), and Wistar rats from both control and hypertensive groups were treated with curcumin (50 or 100 mg/kg/day; gavage) or vehicle for 14 days. Blood and kidneys were collected to determine serum creatinine levels, histological alterations, oxidative stress, MMPs expression and activity, and ED1 expression. <span>l</span>-NAME increased blood pressure, but both doses of curcumin treatment reduced these values. <span>l</span>-NAME treatment increased creatinine levels, glomeruli area, Bowman's space, kidney MMP-2 activity, as well as MMP-9 and ED1 expression, and reduced the number of glomeruli. Curcumin treatment prevented the increase in creatinine levels, MMP-2 activity, and reduced MMP-2, MMP-9, ED1, and superoxide levels, as well as increased superoxide dismutase activity and partially prevented glomeruli alterations. Moreover, curcumin directly inhibited MMP-2 activity in vitro. Thus, our main findings demonstrate that curcumin reduced <span>l</span>-NAME-induced hypertension and renal glomerular alterations, inhibited MMP-2 and MMP-9 expression/activity, and reduced oxidative stress and inflammatory processes, which may indirectly impact hypertension-induced renal outcomes.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Valsartan Rescues Suppressed Mitochondrial Metabolism during Insulin Resistance in C2C12 Myotubes 缬沙坦可修复 C2C12 肌管胰岛素抵抗期间受抑制的线粒体代谢

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-07 DOI: 10.1002/cbf.4117

Emily C. Wyatt, Lindsey R. VanDerStad, Norah E. Cook, Macey R. McGovern, Toheed Zaman, Pamela M. Lundin, Roger A. Vaughan

{"title":"Valsartan Rescues Suppressed Mitochondrial Metabolism during Insulin Resistance in C2C12 Myotubes","authors":"Emily C. Wyatt, Lindsey R. VanDerStad, Norah E. Cook, Macey R. McGovern, Toheed Zaman, Pamela M. Lundin, Roger A. Vaughan","doi":"10.1002/cbf.4117","DOIUrl":"10.1002/cbf.4117","url":null,"abstract":"<p>Elevated circulating branched-chain amino acids (BCAA) have been linked with the severity of insulin resistance across numerous populations, implicating heightened BCAA metabolism as a potential therapy for insulin resistance. Recently, the angiotensin II type 1 receptor (AT1R) inhibitor Valsartan (VAL) was identified as a potent inhibitor of branched-chain alpha-keto acid dehydrogenase kinase (BCKDK), a negative regulator of BCAA metabolism. This work investigated the effect of VAL on myotube metabolism and insulin sensitivity under both insulin sensitive and insulin resistant conditions. C2C12 myotubes were treated with or without VAL at 8 µM for 24 h, both with and without hyperinsulinemic-induced insulin resistance. Oxygen consumption and extracellular acidification were used to measure mitochondrial and glycolytic metabolism, respectively. Gene expression was assessed via qRT-PCR, and insulin sensitivity was assessed via Western blot. Insulin resistance significantly reduced both basal and peak mitochondrial function which were rescued to control levels by concurrent VAL. Changes in mitochondrial function occurred without substantial changes in mitochondrial content or related gene expression. Insulin sensitivity and glycolytic metabolism were unaffected by VAL, as was lipogenic signaling and lipid content. Additionally, both VAL and insulin resistance depressed <i>Bckdha</i> expression. Interestingly, an interaction effect was observed for extracellular isoleucine, valine, and total BCAA (but not leucine), suggesting VAL may alter BCAA utilization in an insulin sensitivity-dependent manner. Insulin resistance appears to suppress mitochondrial function in a myotube model which can be rescued by VAL. Further research will be required to explore the implications of these findings in more complex models.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.4117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hepatocellular Interactions of Potential Nutraceuticals in the Management of Inflammatory NAFLD 治疗炎症性非酒精性脂肪肝的潜在营养保健品的肝细胞相互作用。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-05 DOI: 10.1002/cbf.4112

Devaraj Ezhilarasan, Kulanthaivel Langeswaran

{"title":"Hepatocellular Interactions of Potential Nutraceuticals in the Management of Inflammatory NAFLD","authors":"Devaraj Ezhilarasan, Kulanthaivel Langeswaran","doi":"10.1002/cbf.4112","DOIUrl":"10.1002/cbf.4112","url":null,"abstract":"<div>\u0000 \u0000 <p>Numerous studies highlight the potential of natural antioxidants, such as those found in foods and plants, to prevent or treat nonalcoholic fatty liver disease (NAFLD). Inflammation is a key factor in the progression from high-fat diet-induced NAFLD to nonalcoholic steatohepatitis (NASH). Injured liver cells and immune cells release inflammatory cytokines, activating hepatic stellate cells. These cells acquire a profibrogenic phenotype, leading to extracellular matrix accumulation and fibrosis. Persistent fibrosis can progress to cirrhosis. Fatty infiltration, oxidative stress, and inflammation exacerbate fatty liver diseases. Thus, many plant-derived antioxidants, like silymarin, silibinin, curcumin, resveratrol, berberine, and quercetin, have been extensively studied in experimental models and clinical patients with NAFLD. Experimentally, these compounds have shown beneficial effects in reducing lipid accumulation, oxidative stress, and inflammatory markers by modulating the ERK, NF-κB, AMPKα, and PPARγ pathways. They also help decrease metabolic endotoxemia, intestinal permeability, and gut inflammation. Clinically, silymarin and silibinin have been found to reduce transaminase levels, while resveratrol and curcumin help alleviate inflammation in NAFLD patients. However, these phytocompounds exhibit poor water solubility, leading to low oral bioavailability and hindering their biological efficacy. Additionally, inconclusive clinical results highlight the need for further trials with larger populations, longer durations, and standardized protocols.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reciprocal Interactions Between Apelin and Noncoding RNAs in Cancer Progression 癌症进展过程中 Apelin 与非编码 RNA 之间的相互影响

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-04 DOI: 10.1002/cbf.4116

Abdollah Jafarzadeh, Bahar Naseri, Hossein Khorramdelazad, Sara Jafarzadeh, Farid Ghorbaninezhad, Zeynab Asgari, Javad Masoumi, Maryam Nemati

{"title":"Reciprocal Interactions Between Apelin and Noncoding RNAs in Cancer Progression","authors":"Abdollah Jafarzadeh, Bahar Naseri, Hossein Khorramdelazad, Sara Jafarzadeh, Farid Ghorbaninezhad, Zeynab Asgari, Javad Masoumi, Maryam Nemati","doi":"10.1002/cbf.4116","DOIUrl":"10.1002/cbf.4116","url":null,"abstract":"<div>\u0000 \u0000 <p>Apelin, a bioactive peptide that serves as an endogenous ligand for the apelin receptor (APJ), is overexpressed in various types of cancers and contributes to cancer cell proliferation, viability, migration, angiogenesis, and metastasis, as well as immune deviation. Noncoding RNAs (ncRNAs) regulate gene expression, and there is growing evidence suggesting a bidirectional crosstalk between ncRNAs (including long noncoding RNAs [lncRNAs], circular RNAs [circRNAs], and microRNAs [miRNAs]) and apelin in cancers. Certain miRNAs can directly target the apelin and inhibit its expression, thereby suppressing tumor growth. It has been indicated that miR-224, miR-195/miR-195-5p, miR-204-5p, miR-631, miR-4286, miR-637, miR-4493, and miR-214-3p target apelin mRNA and influence its expression in prostate cancer, lung cancer, esophageal cancer, chondrosarcoma, melanoma, gastric cancer, glioma, and hepatocellular carcinoma (HCC), respectively. Moreover, circ-NOTCH1, circ-ZNF264, and lncRNA BACE1-AS upregulate apelin expression in gastric cancer, glioma, and HCC, respectively. On the other hand, apelin has been shown to regulate the expression of certain ncRNAs to affect tumorigenesis. It was revealed that apelin affects the expression of circ_0000004/miR-1303, miR-15a-5p, and miR-106a-5p in osteosarcoma, lung cancer, and prostate cancer, respectively. This review explains a bidirectional interplay between ncRNAs and apelin in cancers to provide insights concerning the molecular mechanisms underlying this crosstalk and potential implications for cancer therapy.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gut microbiota derived short-chain fatty acids in physiology and pathology: An update 肠道微生物群衍生的短链脂肪酸在生理学和病理学中的作用：最新进展。

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-03 DOI: 10.1002/cbf.4108

Archana, Abhijeet Kumar Gupta, Ashab Noumani, Dharmendra Kumar Panday, Fareen Zaidi, Gaurav Kumar Sahu, Gunjan Joshi, Manisha Yadav, Shikha Jyoti Borah, Vanne Susmitha, Anand Mohan, Anil Kumar, Pratima R. Solanki

{"title":"Gut microbiota derived short-chain fatty acids in physiology and pathology: An update","authors":"Archana, Abhijeet Kumar Gupta, Ashab Noumani, Dharmendra Kumar Panday, Fareen Zaidi, Gaurav Kumar Sahu, Gunjan Joshi, Manisha Yadav, Shikha Jyoti Borah, Vanne Susmitha, Anand Mohan, Anil Kumar, Pratima R. Solanki","doi":"10.1002/cbf.4108","DOIUrl":"10.1002/cbf.4108","url":null,"abstract":"<p>Short-chain fatty acids (SCFAs) are essential molecules produced by gut bacteria that fuel intestinal cells and may also influence overall health. An imbalance of SCFAs can result in various acute and chronic diseases, including diabetes, obesity and colorectal cancer (CRC). This review delves into the multifaceted roles of SCFAs, including a brief discussion on their source and various gut-residing bacteria. Primary techniques used for detection of SCFAs, including gas chromatography, high-performance gas chromatography, nuclear magnetic resonance and capillary electrophoresis are also discussed through this article. This review study also compiles various synthesis pathways of SCFAs from diverse substrates such as sugar, acetone, ethanol and amino acids. The different pathways through which SCFAs enter cells for immune response regulation are also highlighted. A major emphasis is the discussion on diseases associated with SCFA dysregulation, such as anaemia, brain development, CRC, depression, obesity and diabetes. This includes exploring the relationship between SCFA levels across ethnicities and their connection with blood pressure and CRC. In conclusion, this review highlights the critical role of SCFAs in maintaining gut health and their implications in various diseases, emphasizing the need for further research on SCFA detection, synthesis and their potential as diagnostic biomarkers. Future studies of SCFAs will pave the way for the development of novel diagnostic tools and therapeutic strategies for optimizing gut health and preventing diseases associated with SCFA dysregulation.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Association Between Type 2 Diabetes Mellitus and Alzheimer's Disease: Common Molecular Mechanism and Therapeutic Targets 2 型糖尿病与阿尔茨海默病之间的关联：共同的分子机制和治疗靶点

IF 2.8 3区生物学

Cell Biochemistry and Function Pub Date : 2024-09-03 DOI: 10.1002/cbf.4111

Aparna Chauhan, Sachin Dubey, Smita Jain

{"title":"Association Between Type 2 Diabetes Mellitus and Alzheimer's Disease: Common Molecular Mechanism and Therapeutic Targets","authors":"Aparna Chauhan, Sachin Dubey, Smita Jain","doi":"10.1002/cbf.4111","DOIUrl":"10.1002/cbf.4111","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetes mellitus (DM) and Alzheimer's disease (AD) rates are rising, mirroring the global trend of an aging population. Numerous epidemiological studies have shown that those with Type 2 diabetes (T2DM) have an increased risk of developing dementia. These degenerative and progressive diseases share some risk factors. To a large extent, the amyloid cascade is responsible for AD development. Neurofibrillary tangles induce neurodegeneration and brain atrophy; this chain reaction begins with hyperphosphorylation of tau proteins caused by progressive amyloid beta (Aβ) accumulation. In addition to these processes, it seems that alterations in brain glucose metabolism and insulin signalling lead to cell death and reduced synaptic plasticity in AD, before the onset of symptoms, which may be years away. Due to the substantial evidence linking insulin resistance in the brain with AD, researchers have coined the name “Type 3 diabetes” to characterize the condition. We still know little about the processes involved, even though current animal models have helped illuminate the links between T2DM and AD. This brief overview discusses insulin and IGF-1 signalling disorders and the primary molecular pathways that may connect them. The presence of GSK-3β in AD is intriguing. These proteins' association with T2DM and pancreatic β-cell failure suggests they might be therapeutic targets for both disorders.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"42 7","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0