Molecular and Cellular Biochemistry最新文献

RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade. RIP3通过调节AKT/Nrf2信号级联，在多柔比星诱导的心脏毒性中协调氧化应激和脓毒症。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-07-02 DOI: 10.1007/s11010-024-05029-6

Zhenyi Wang, Yitong Yang, Nisha Wang, Linhe Lu, Chennian Xu, Jun Ren, Lifang Yang

{"title":"RIP3 orchestrates oxidative stress and pyroptosis in doxorubicin-induced cardiotoxicity through regulation of AKT/Nrf2 signaling cascade.","authors":"Zhenyi Wang, Yitong Yang, Nisha Wang, Linhe Lu, Chennian Xu, Jun Ren, Lifang Yang","doi":"10.1007/s11010-024-05029-6","DOIUrl":"10.1007/s11010-024-05029-6","url":null,"abstract":"This study was designed to explore the role of RIP3 in DOX-induced cardiotoxicity and its underlying molecular mechanisms. Our results demonstrate that RIP3 exacerbates DOX-induced cardiotoxicity through promoting oxidative stress and pyroptosis by regulating the AKT/Nuclear factor erythroid 2-related factor 2 (Nrf2) signal pathway. Inhibition of RIP3 using GSK-872 attenuated DOX-induced cardiac remodeling and contractile dysfunction. Moreover, using GSK-872 in vivo, the results revealed that inhibition of RIP3 alleviated DOX-induced cardiotoxicity by the resulting inhibition of oxidative stress and pyroptosis. In addition, inhibition of RIP3 increased the protein levels of AKT and Nrf2 in DOX-treated mouse hearts. Furthermore, the AKT inhibitor LY294002 lessened RIP3 reduction-offered protection against DOX-induced H9c2 cell injury by moderating oxidative stress and pyroptosis. Taken together, these data demonstrate that RIP3 activation orchestrates DOX-induced cardiotoxicity through elevated oxidative stress and pyroptosis in an AKT/Nrf2-dependent manner. Those findings highlight the clinical relevance and therapeutic potential of targeting RIP3 for the treatment of DOX-induced cardiotoxicity.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2331-2343"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Dietary salt promotes cognitive impairment through repression of SIRT3/PINK1-mediated mitophagy and fission. 膳食盐通过抑制SIRT3/PINK1介导的有丝分裂和分裂，促进认知障碍。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-07-13 DOI: 10.1007/s11010-024-05069-y

Haixia Fan, Minghao Yuan, Shenyuan Wang, Xu Yang, Liu Shu, Yinshuang Pu, Qian Zou, Xiaogang Zhang, Chuanling Wang, Zhiyou Cai

{"title":"Dietary salt promotes cognitive impairment through repression of SIRT3/PINK1-mediated mitophagy and fission.","authors":"Haixia Fan, Minghao Yuan, Shenyuan Wang, Xu Yang, Liu Shu, Yinshuang Pu, Qian Zou, Xiaogang Zhang, Chuanling Wang, Zhiyou Cai","doi":"10.1007/s11010-024-05069-y","DOIUrl":"10.1007/s11010-024-05069-y","url":null,"abstract":"Dietary salt is increasingly recognized as an independent risk factor for cognitive impairment. However, the exact mechanisms are not yet fully understood. Mitochondria, which play a crucial role in energy metabolism, are implicated in cognitive function through processes such as mitochondrial dynamics and mitophagy. While mitochondrial dysfunction is acknowledged as a significant determinant of cognitive function, the specific relationship between salt-induced cognitive impairment and mitochondrial health has yet to be fully elucidated. Here, we explored the underlying mechanism of cognitive impairment of mice and N2a cells treated with high-salt focusing on the mitochondrial homeostasis with western blotting, immunofluorescence, electron microscopy, RNA sequencing, and more. We further explored the potential role of SIRT3 in salt-induced mitochondrial dysfunction and synaptic alteration through plasmid transfection and siRNA. High salt diet significantly inhibited mitochondrial fission and blocked mitophagy, leading to dysfunctional mitochondria and impaired synaptic plasticity. Our findings demonstrated that SIRT3 not only promote mitochondrial fission by modulating phosphorylated DRP1, but also rescue mitophagy through promoting PINK1/Parkin-dependent pathway. Overall, our data for the first time indicate that mitochondrial homeostasis imbalance is a driver of impaired synaptic plasticity in a cognitive impairment phenotype that is exacerbated by a long-term high-salt diet, and highlight the protective role of SIRT3 in this process.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2345-2360"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141600584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

MicroRNA-205-5p inhibits the growth and migration of breast cancer through targeting Wnt/β-catenin co-receptor LRP6 and interacting with lncRNAs. MicroRNA-205-5p通过靶向Wnt/β-catenin共受体LRP6和与lncRNA相互作用抑制乳腺癌的生长和迁移。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-10-26 DOI: 10.1007/s11010-024-05136-4

Sameh H Mohamed, Mohamed M Kamal, Ahmed M Reda, Noha M Mesbah, Dina M Abo-Elmatty, Asmaa R Abdel-Hamed

{"title":"MicroRNA-205-5p inhibits the growth and migration of breast cancer through targeting Wnt/β-catenin co-receptor LRP6 and interacting with lncRNAs.","authors":"Sameh H Mohamed, Mohamed M Kamal, Ahmed M Reda, Noha M Mesbah, Dina M Abo-Elmatty, Asmaa R Abdel-Hamed","doi":"10.1007/s11010-024-05136-4","DOIUrl":"10.1007/s11010-024-05136-4","url":null,"abstract":"Breast cancer is the most prevalent type of cancer among women worldwide. Non-coding RNAs play a fundamental role in regulating the expression of different genes. MicroRNAs (miRNAs) are known to bind to mRNA and either induce its degradation or repress its translation. Also, miRNA can modulate the expression of long non-coding RNAs (lncRNA) through different mechanisms. This study aims to determine the role of miRNA-205-5p in breast cancer cell lines. miR-205-5p was bioinformatically predicted to interact with LRP6 mRNA and lncRNAs MALAT1, NEAT1, SNHG5, and SNHG16. Then, the levels of miR-205-5p and its target genes and lncRNAs in breast cancer cell lines MCF-7 and MDA-MB-231 were determined. In addition, MCF-7 and MDA-MB-231 breast cancer cells were transfected with miR-205-5p mimic or miRNA mimic negative control using lipofectamine 3000, and the effect of miR-205-5p overexpression on cellular proliferation and migration was assessed. Moreover, we probed the impact of miR-205-5p overexpression on the expression levels of LRP6, Wnt/β-catenin pathway genes, lncRNAs, and apoptotic markers. miR-205-5p upregulation resulted in decreasing the growth and migration and induced apoptosis markers in the two tested breast cancer subtypes. Additionally, miR-205-5p overexpression resulted in decreasing the expression of LRP6 in MCF-7 and MDA-MB-231 cells leading to downregulation of Wnt/β-catenin target genes, c-Myc, cyclin D1, and PPARδ and had various regulatory effects on the expression of lncRNAs MALAT1, NEAT1, SNHG5, and SNHG16. miR-205-5p inhibits the proliferation and migration of breast cancer through diverse mechanisms including targeting LRP6, Wnt/β-catenin pathway, and its regulatory effects on lncRNAs.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2117-2129"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mitochondrial Dysfunction-Molecular Mechanisms and Potential Treatment approaches of Hepatocellular Carcinoma. 线粒体功能障碍--肝细胞癌的分子机制和潜在治疗方法。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-10-27 DOI: 10.1007/s11010-024-05144-4

Lianlin Zeng, Lutao Zhu, Shasha Fu, Yangan Li, Kehui Hu

{"title":"Mitochondrial Dysfunction-Molecular Mechanisms and Potential Treatment approaches of Hepatocellular Carcinoma.","authors":"Lianlin Zeng, Lutao Zhu, Shasha Fu, Yangan Li, Kehui Hu","doi":"10.1007/s11010-024-05144-4","DOIUrl":"10.1007/s11010-024-05144-4","url":null,"abstract":"Primary liver cancer (PLC), also known as hepatocellular carcinoma (HCC), is a common type of malignant tumor of the digestive system. Its pathological form has a significant negative impact on the patients' quality of life and ability to work, as well as a significant financial burden on society. Current researches had identified chronic hepatitis B virus infection, aflatoxin B1 exposure, and metabolic dysfunction-associated steatotic liver disease (MASLD) as the main causative factors of HCC. Numerous variables, including inflammatory ones, oxidative stress, apoptosis, autophagy, and others, have been linked to the pathophysiology of HCC. On the other hand, autoimmune regulation, inflammatory response, senescence of the hepatocytes, and mitochondrial dysfunction are all closely related to the pathogenesis of HCC. In fact, a growing number of studies have suggested that mitochondrial dysfunction in hepatocytes may be a key factor in the pathogenesis of HCC. In disorders linked to cancer, mitochondrial dysfunction has gained attention in recent 10 years. As the primary producer of adenosine triphosphate (ATP) in liver cells, mitochondria are essential for preserving cell viability and physiological processes. By influencing multiple pathological processes, including mitochondrial fission/fusion, mitophagy, cellular senescence, and cell death, mitochondrial dysfunction contributes to the development of HCC. We review the molecular mechanisms of HCC-associated mitochondrial dysfunction and discuss new directions for quality control of mitochondrial disorders as a treatment for HCC.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2131-2142"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity. 解密细胞和细胞外非编码 RNA 在化疗诱导的心脏毒性中的作用。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-11-01 DOI: 10.1007/s11010-024-05143-5

Pan Feng, Fan Yang, Dongmei Zang, Dapeng Bai, Liyan Xu, Yueyun Fu, Ranran You, Tao Liu, Xinyu Yang

{"title":"Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity.","authors":"Pan Feng, Fan Yang, Dongmei Zang, Dapeng Bai, Liyan Xu, Yueyun Fu, Ranran You, Tao Liu, Xinyu Yang","doi":"10.1007/s11010-024-05143-5","DOIUrl":"10.1007/s11010-024-05143-5","url":null,"abstract":"Chemotherapy-induced cardiotoxicity is a major adverse effect, driven by multiple factors in its pathogenesis. Notably, RNAs have emerged as significant contributors in both cancer and heart failure (HF). RNAs carry genetic and metabolic information that mirrors the current state of cells, making them valuable as potential biomarkers and therapeutic tools for diagnosing, predicting, and treating a range of diseases, including cardiotoxicity. Over 97% of the genome is transcribed into non-coding RNAs (ncRNAs), including ribosomal RNA (rRNAs), transfer RNAs (tRNAs), and newly identified microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs). NcRNAs function not only within their originating cells but also in recipient cells by being transported through extracellular compartments, referred to as extracellular RNAs (exRNAs). Since ncRNAs were identified as key regulators of gene expression, numerous studies have highlighted their significance in both cancer and cardiovascular diseases. Nevertheless, the role of ncRNAs in cardiotoxicity remains not fully elucidated. The study aims to review the existing knowledge on ncRNAs in Cardio-Oncology and explore the potential of ncRNA-based biomarkers and therapies. These investigations could advance the clinical application of ncRNA research, improving early detection and mitigating of chemotherapy-induced cardiotoxicity.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2177-2199"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Carbon monoxide-releasing molecule-3 ameliorates traumatic brain injury-induced cardiac dysfunctions via inhibition of pyroptosis and apoptosis. 一氧化碳释放分子-3可通过抑制热凋亡和细胞凋亡改善创伤性脑损伤引起的心脏功能障碍。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-10-08 DOI: 10.1007/s11010-024-05130-w

Jing Bai, Wen-Bo Sun, Wei-Chao Zheng, Xu-Peng Wang, Yang Bai

{"title":"Carbon monoxide-releasing molecule-3 ameliorates traumatic brain injury-induced cardiac dysfunctions via inhibition of pyroptosis and apoptosis.","authors":"Jing Bai, Wen-Bo Sun, Wei-Chao Zheng, Xu-Peng Wang, Yang Bai","doi":"10.1007/s11010-024-05130-w","DOIUrl":"10.1007/s11010-024-05130-w","url":null,"abstract":"Traumatic brain injury (TBI) frequently results in cardiac dysfunction and impacts the quality of survivors' life. It has been reported that carbon monoxide-releasing molecule-3 (CORM-3) administration immediately after hemorrhagic shock and resuscitation (HSR) ameliorated the HSR‑induced cardiac dysfunctions. The purpose of this study was to determine whether the application of CORM-3 on TBI exerted therapeutic effects against TBI-induced cardiac dysfunctions. Rats were randomly divided into four groups (n = 12) including Sham, TBI, TBI/CORM-3 and TBI/inactive CORM-3 (iCORM-3) groups. TBI was established by a weight-drop model. The rats in the TBI/CORM-3 group and TBI/iCORM-3 group were intravenously injected with CORM-3 and iCORM-3 (4 mg/kg) following TBI, respectively. The time of death in the rats that did not survive within 24 h was recorded. 24 h post-trauma, the cardiac function, pathological change, serum troponin T and creatine kinase-MB (CK-MB) levels, pyroptosis, apoptosis and expressions of TUNEL staining, Gasdermin D (GSDMD), IL-1β, IL-18, ratio Bax/Bcl-2 were assessed by echocardiography, hematoxylin-eosin staining, chemiluminescence, immunofluorescence, and western blot assays, respectively. TBI-treated rats exhibited dramatically decreased ejection fraction and aggravated myocardial injury, increased mortality rate, elevated levels of serum troponin T and CK-MB, promoted cardiac pyroptosis and apoptosis, and upregulated expressions of cleaved caspase-3, GSDMD N-terminal fragments, IL-1β, IL-18, and ratio of Bax/Bcl-2, whereas CORM-3 partially reversed these changes. CORM-3 ameliorated TBI-induced cardiac injury and dysfunction. This mechanism may be responsible for the inhibition of pyroptosis and apoptosis in cardiomyocyte.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2501-2509"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

A new gold(I) phosphine complex induces apoptosis in prostate cancer cells by increasing reactive oxygen species. 一种新型金（I）膦复合物通过增加活性氧诱导前列腺癌细胞凋亡。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-05-24 DOI: 10.1007/s11010-024-05035-8

Yuan Wang, Haokun Yuan, Ruiqin Fang, Junzhu Lu, Jiaqi Duo, Ge Li, Wei-Jia Wang

{"title":"A new gold(I) phosphine complex induces apoptosis in prostate cancer cells by increasing reactive oxygen species.","authors":"Yuan Wang, Haokun Yuan, Ruiqin Fang, Junzhu Lu, Jiaqi Duo, Ge Li, Wei-Jia Wang","doi":"10.1007/s11010-024-05035-8","DOIUrl":"10.1007/s11010-024-05035-8","url":null,"abstract":"Thioredoxin reductase (TrxR) is a pivotal regulator of redox homeostasis. It is frequently overexpressed in various cancer cells, including prostate cancer, making it a promising target for the development of anti-cancer drugs. In this study, we screened a series of newly designed complexes of gold(I) phosphine. Specifically, Compound 5 exhibited the highest cytotoxicity against prostate cancer cells and demonstrated stronger antitumor effects than commonly used drugs, such as cisplatin and auranofin. Importantly, our mechanistic study revealed that Compound 5 effectively inhibits the TrxR system in vitro. Additionally, Compound 5 promoted intracellular accumulation of reactive oxygen species (ROS), leading to mitochondrial dysfunction and irreversible apoptosis in prostate cancer cells. Our in vivo xenograft study further demonstrated that Compound 5 has excellent antitumor activity against prostate cancer cells, but does not cause severe side effects. These findings provide a promising lead Compound for the development of novel antitumor agents targeting prostate cancer and offer a valuable tool for investigating biological pathways involving TrxR and ROS modulation.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2265-2276"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The truncated AXIN1 isoform promotes hepatocellular carcinoma metastasis through SRSF9-mediated exon 9 skipping. 截短的 AXIN1 异构体通过 SRSF9 介导的第 9 号外显子跳越促进肝细胞癌转移。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-05-15 DOI: 10.1007/s11010-024-05012-1

Qian-Qian Zhang, Ying-Shuang Miao, Jun-Yi Hu, Rui-Xuan Liu, Yue-Xiao Hu, Feng Wang

{"title":"The truncated AXIN1 isoform promotes hepatocellular carcinoma metastasis through SRSF9-mediated exon 9 skipping.","authors":"Qian-Qian Zhang, Ying-Shuang Miao, Jun-Yi Hu, Rui-Xuan Liu, Yue-Xiao Hu, Feng Wang","doi":"10.1007/s11010-024-05012-1","DOIUrl":"10.1007/s11010-024-05012-1","url":null,"abstract":"Axis inhibitor protein 1 (AXIN1) is a protein recognized for inhibiting tumor growth and is commonly involved in cancer development. In this study, we explored the potential molecular mechanisms that connect alternative splicing of AXIN1 to the metastasis of hepatocellular carcinoma (HCC). Transcriptome sequencing, RT‒PCR, qPCR and Western blotting were utilized to determine the expression levels of AXIN1 in human HCC tissues and HCC cells. The effects of the AXIN1 exon 9 alternative splice isoform and SRSF9 on the migration and invasion of HCC cells were assessed through wound healing and Transwell assays, respectively. The interaction between SRSF9 and AXIN1 was investigated using UV crosslink RNA immunoprecipitation, RNA pulldown, and RNA immunoprecipitation assays. Furthermore, the involvement of the AXIN1 isoform and SRSF9 in HCC metastasis was validated in a nude mouse model. AXIN1-L (exon 9 including) expression was downregulated, while AXIN1-S (exon 9 skipping) was upregulated in HCC. SRSF9 promotes the production of AXIN1-S by interacting with the sequence of exons 8 and 10 of AXIN1. AXIN1-S significantly promoted HCC cells migration and invasion by activating the Wnt pathway, while the opposite effects were observed for AXIN1-L. In vivo experiments demonstrated that AXIN1-L inhibited HCC metastasis, whereas SRSF9 promoted HCC metastasis in part by regulating the level of AXIN1-S. AXIN1, a tumor suppressor protein that targets the AXIN1/Wnt/β-catenin signaling axis, may be a promising prognostic factor and a valuable therapeutic target for HCC.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2247-2263"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140920774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians. 肾素血管紧张素系统诱发的肌肉萎缩：假定机制及对临床医生的影响。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-05-29 DOI: 10.1007/s11010-024-05043-8

Baris Afsar, Rengin Elsurer Afsar, Yasar Caliskan, Krista L Lentine, John C Edwards

{"title":"Renin angiotensin system-induced muscle wasting: putative mechanisms and implications for clinicians.","authors":"Baris Afsar, Rengin Elsurer Afsar, Yasar Caliskan, Krista L Lentine, John C Edwards","doi":"10.1007/s11010-024-05043-8","DOIUrl":"10.1007/s11010-024-05043-8","url":null,"abstract":"Renin angiotensin system (RAS) alters various mechanisms related to muscle wasting. The RAS system consists of classical and non-classical pathways, which mostly function differently. Classical RAS pathway, operates through angiotensin II (AngII) and angiotensin type 1 receptors, is associated with muscle wasting and sarcopenia. On the other hand, the non-classical RAS pathway, which operates through angiotensin 1-7 and Mas receptor, is protective against sarcopenia. The classical RAS pathway might induce muscle wasting by variety of mechanisms. AngII reduces body weight, via reduction in food intake, possibly by decreasing hypothalamic expression of orexin and neuropeptide Y, insulin like growth factor-1 (IGF-1) and mammalian target of rapamycin (mTOR), signaling, AngII increases skeletal muscle proteolysis by forkhead box transcription factors (FOXO), caspase activation and muscle RING-finger protein-1 transcription. Furthermore, AngII infusion in skeletal muscle reduces phospho-Bad (Ser136) expression and induces apoptosis through increased cytochrome c release and DNA fragmentation. Additionally, Renin angiotensin system activation through AT1R and AngII stimulates tumor necrosis factor-α, and interleukin-6 which induces muscle wasting, Last but not least classical RAS pathway, induce oxidative stress, disturb mitochondrial energy metabolism, and muscle satellite cells which all lead to muscle wasting and decrease muscle regeneration. On the contrary, the non-classical RAS pathway functions oppositely to mitigate these mechanisms and protects against muscle wasting. In this review, we summarize the mechanisms of RAS-induced muscle wasting and putative implications for clinical practice. We also emphasize the areas of uncertainties and suggest potential research areas.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"1935-1949"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141174861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The role of hydrogen sulfide in the regulation of necroptosis across various pathological processes. 硫化氢在调节各种病理过程中的坏死过程中的作用。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2025-04-01 Epub Date: 2024-08-14 DOI: 10.1007/s11010-024-05090-1

Shiyun Guo, Yanting Zhang, Jingwen Lian, Chunqi Su, Honggang Wang

{"title":"The role of hydrogen sulfide in the regulation of necroptosis across various pathological processes.","authors":"Shiyun Guo, Yanting Zhang, Jingwen Lian, Chunqi Su, Honggang Wang","doi":"10.1007/s11010-024-05090-1","DOIUrl":"10.1007/s11010-024-05090-1","url":null,"abstract":"Necroptosis is a programmed cell death form executed by receptor-interacting protein kinase (RIPK) 1, RIPK3 and mixed lineage kinase domain-like protein (MLKL), which assemble into an oligomer called necrosome. Accumulating evidence reveals that necroptosis participates in many types of pathological processes. Hence, clarifying the mechanism of necroptosis in pathological processes is particularly important for the prevention and treatment of various diseases. For over 300 years, hydrogen sulfide (H2S) has been widely known in the scientific community as a toxic and foul-smelling gas. However, after discovering the important physiological and pathological functions of H2S, human understanding of this small molecule changed, believing that H2S is the third gas signaling molecule after carbon monoxide (CO) and nitric oxide (NO). H2S plays an important role in various diseases, but the related mechanisms are not yet fully understood. In recent years, more and more studies have shown that H2S regulation of necroptosis is involved in various pathological processes. Herein, we focus on the recent progress on the role of H2S regulation of necroptosis in different pathological processes and profoundly analyze the related mechanisms.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"1999-2013"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141976137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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