Cell Cycle最新文献

Growth hormone suppression in endothelial dysfunction. 内皮功能障碍中的生长激素抑制。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-07-11 DOI: 10.1080/15384101.2025.2531893

Nektarios Barabutis

引用次数: 0

SKP2 E3 ligase in urological malignancies: a critical regulator of the cell cycle and therapeutic target. SKP2 E3连接酶在泌尿系统恶性肿瘤中的作用：细胞周期的关键调节因子和治疗靶点。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-07-03 DOI: 10.1080/15384101.2025.2526211

Mohannad Natheef AbuHaweeleh, Lubna Therachiyil, Kirti S Prabhu, Omar M Khan, Shahab Uddin

引用次数: 0

FAM3A: a novel mitochondrial protein for the treatment of ischemic diseases. FAM3A：一种治疗缺血性疾病的新型线粒体蛋白。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-07-03 DOI: 10.1080/15384101.2025.2527777

Ye Su, Xinggang Cui, Mei Li, Duzhe Jiang, Rui Chen, Ye Zhou

{"title":"FAM3A: a novel mitochondrial protein for the treatment of ischemic diseases.","authors":"Ye Su, Xinggang Cui, Mei Li, Duzhe Jiang, Rui Chen, Ye Zhou","doi":"10.1080/15384101.2025.2527777","DOIUrl":"https://doi.org/10.1080/15384101.2025.2527777","url":null,"abstract":"FAM3 metabolism-regulating signaling molecule A (FAM3A) is a mitochondrial protein belonging to the FAM3 gene family with the potential for the treatment of ischemic diseases. FAM3A promotes adenosine triphosphate (ATP) production and improves mitochondrial function by increasing ATP synthase activity and activating the protein kinase B-cyclic AMP-responsive element binding protein-forkhead box D3-ATP synthase regulatory loop, thereby reducing reactive oxygen species production and inhibiting oxidative stress-induced cell death. Additionally, FAM3A activates the nuclear factor erythroid 2-related factor 2 signaling pathway and upregulates the expression of antioxidant proteins, further enhancing the cellular oxidative defense capacity. During angiogenesis, FAM3A positively regulates vascular endothelial growth factor A and promotes endothelial cell migration, proliferation, and tube formation. FAM3A is closely related to atherosclerosis, ischemic encephalopathy, liver ischemia - reperfusion injury, myocardial ischemia, and acute kidney injury. FAM3A plays a role in the course of these diseases via multiple mechanisms, including the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, effectively reducing the inflammatory response and oxidative stress, and influencing disease development. This review comprehensively examines the role of FAM3A in the pathophysiological processes of ischemic diseases across various organs.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-15"},"PeriodicalIF":3.4,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559311","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

Correction. 修正。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-06-10 DOI: 10.1080/15384101.2025.2513567

引用次数: 0

M2 macrophages promote PKM2 production in fibroblasts to alleviate UVB-induced photoaging. M2巨噬细胞促进成纤维细胞PKM2的产生，减轻uvb诱导的光老化。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-06-05 DOI: 10.1080/15384101.2025.2514988

Shanshan Jia, Nian Shi, Meiqi Lu, Xiaoyang Wang, Yongjun Qi, Xiaochuan Wang, Jie Zhao, Duyin Jiang

引用次数: 0

Hair-follicle-associated pluripotent (HAP) stem-cell-sheet implantation accelerates cutaneous wound closure and suppresses scar formation in a mouse model. 在小鼠模型中，毛囊相关多能干细胞片植入加速皮肤伤口愈合并抑制疤痕形成。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-27 DOI: 10.1080/15384101.2025.2508112

Koya Obara, Kyoko Baba, Kyoumi Shirai, Yuko Hamada, Nobuko Arakawa, Ayami Hasegawa, Nanako Takaoka, Ryoichi Aki, Robert M Hoffman

{"title":"Hair-follicle-associated pluripotent (HAP) stem-cell-sheet implantation accelerates cutaneous wound closure and suppresses scar formation in a mouse model.","authors":"Koya Obara, Kyoko Baba, Kyoumi Shirai, Yuko Hamada, Nobuko Arakawa, Ayami Hasegawa, Nanako Takaoka, Ryoichi Aki, Robert M Hoffman","doi":"10.1080/15384101.2025.2508112","DOIUrl":"https://doi.org/10.1080/15384101.2025.2508112","url":null,"abstract":"Patients frequently experience physical, mental, and even financial distress because of acute or chronic skin wounds. In severe situations, scarring on the skin can be quite noticeable, cause persistent discomfort, restrict joint motion, or be mentally taxing. Hair-follicle-associated pluripotent (HAP) stem cells were discovered by our laboratory, in the bulge area of the hair follicle and can differentiate to neurons, glia, beating cardiomyocytes, keratinocytes and nascent vessels. In the present study, HAP stem cell sheets were formed by culturing the upper part of hair follicles and implanting into mice with skin ulcers. The HAP stem cell sheets contained keratinocytes, endothelial cells and neurons. Autologous HAP stem cell sheet implantation to the dorsal wound in C57BL/6J mice significantly accelerated wound closure compared with non-implanted control mice. HAP-stem-cell sheets expressing green fluorescent protein (GFP) implanted into nude mice differentiated into keratinocytes in the epidermis, and neurons and endothelial cells in the dermis. The thicknesses of the epidermis and dermis and M2 macrophage and myofibroblast infiltration into the wound were significantly decreased in HAP-stem cell-implanted mice compared with non-implanted control mice. Expression levels of TGF-β1, COL1A2 and COL3A1 mRNA in the wound were significantly decreased in HAP stem cell-implanted mice compared with non-implanted control mice. These results suggest that implanting HAP stem cell sheets accelerates cutaneous wound closure and suppresses scar formation. The HAP stem cells used in the present study thus have potential as a future clinical strategy for accelerating wound healing.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-14"},"PeriodicalIF":3.4,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155883","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

Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8. 赖氨酸甲基转移酶SET8对BRCA1信号的细胞周期依赖性抑制。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-22 DOI: 10.1080/15384101.2025.2508114

Yannick Perez, Fatima Alhourani, Julie Patouillard, Cyril Ribeyre, Marion Larroque, Véronique Baldin, David Lleres, Charlotte Grimaud, Eric Julien

{"title":"Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8.","authors":"Yannick Perez, Fatima Alhourani, Julie Patouillard, Cyril Ribeyre, Marion Larroque, Véronique Baldin, David Lleres, Charlotte Grimaud, Eric Julien","doi":"10.1080/15384101.2025.2508114","DOIUrl":"10.1080/15384101.2025.2508114","url":null,"abstract":"The cell-cycle regulated methyltransferase SET8 is the sole enzyme responsible for the mono-methylation of histone H4 at lysine 20 (H4K20) that is the substrate for di- and trimethylation mainly by SUV4-20Hs enzymes. Both SET8 and SUV4-20Hs have been implicated in regulating DNA repair pathway choice through the inverse affinities of BRCA1-BARD1 and 53BP1 complexes for disparate methylation states of H4K20. However, the precise and respective functions of each H4K20 methyltransferase in DNA repair pathways remain to be clarified. Here, we show that SET8 acts as a potent chromatin inhibitor of homologous recombination and that its timely degradation during DNA replication is essential for the spontaneous nuclear focal accumulation of BRCA1 and RAD51 complexes during the S phase. Strikingly, the anti-recombinogenic function of SET8 is independent of SUV4-20H activity but requires the subsequent recruitment of the ubiquitin ligase RNF168. Moreover, we show that SET8-induced BRCA1 inhibition is not necessarily related to the loss of BARD1 binding to unmethylated histone H4K20. Instead, it is largely caused by the accumulation of 53BP1 in a manner depending on the concerted activities of SET8 and RNF168 on chromatin. Conversely, the lack of SET8 and H4K20 mono-methylation on newly assembly chromatin after DNA replication led to the untimely accumulation of BRCA1 on chromatin at the subsequent G1 phase. Altogether, these results establish the de novo activity of SET8 on chromatin as a primordial epigenetic lock of the BRCA1-mediated HR pathway during the cell cycle.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-23"},"PeriodicalIF":3.4,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126933","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

Succinate reduces biological activity and mitochondrial function of human adipose-derived stem cells. 琥珀酸盐降低人脂肪干细胞的生物活性和线粒体功能。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-05-20 DOI: 10.1080/15384101.2025.2508109

Bo Wang, Xinxin Wang, Meijin Guo, Huiming Xu

{"title":"Succinate reduces biological activity and mitochondrial function of human adipose-derived stem cells.","authors":"Bo Wang, Xinxin Wang, Meijin Guo, Huiming Xu","doi":"10.1080/15384101.2025.2508109","DOIUrl":"https://doi.org/10.1080/15384101.2025.2508109","url":null,"abstract":"Elevated succinate accumulation has been demonstrated to be associated with metabolic and inflammatory disorders. Our previous study revealed that adipose-derived stem cells (ADSC) from obese individuals exhibit high succinate, reduced biological activity, and mitochondrial dysfunction. However, the precise role of succinate in these processes remains unclear. Here, we investigated the effects of excess succinate on cellular biological activity, immunomodulatory capacity, and mitochondrial function of ADSC. We found that elevated succinate levels in ADSC decreased proliferation and differentiation potential, while promoting M1 macrophage polarization. Furthermore, succinate accumulation impaired mitochondrial biogenesis and metabolism, increasing in reactive oxygen species (ROS) production and inflammatory responses. Transcriptome sequencing analysis further confirmed that succinate upregulated inflammatory pathways, suppressed mitochondrial biogenesis and metabolism, and enhanced cellular apoptosis and senescence, accompanied by reduced DNA replication and repair. Overall, these findings imply that succinate accumulation in ADSC triggers inflammatory response and mitochondrial dysfunction, potentially contributing to a decline of cellular biological activity. Targeting succinate may offer therapeutic potential for metabolic disorders.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-13"},"PeriodicalIF":3.4,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109873","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

The involvement of cyclin-dependent kinase 7 (CDK7) and 9 (CDK9) in coordinating transcription and cell cycle checkpoint regulation. 细胞周期蛋白依赖性激酶7 （CDK7）和9 （CDK9）参与协调转录和细胞周期检查点调节。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-11-01 Epub Date: 2025-04-14 DOI: 10.1080/15384101.2025.2485844

Cheng-Fan Lee, Kenneth J Pienta, Sarah R Amend

{"title":"The involvement of cyclin-dependent kinase 7 (CDK7) and 9 (CDK9) in coordinating transcription and cell cycle checkpoint regulation.","authors":"Cheng-Fan Lee, Kenneth J Pienta, Sarah R Amend","doi":"10.1080/15384101.2025.2485844","DOIUrl":"10.1080/15384101.2025.2485844","url":null,"abstract":"Cells regulate the expression of cell cycle-related genes, including cyclins essential for mitosis, through the transcriptional activity of the positive transcription elongation factor b (P-TEFb), a complex comprising CDK9, cyclin T, and transcription factors. P-TEFb cooperates with CDK7 to activate RNA polymerase. In response to DNA stress, the cell cycle shifts from mitosis to repair, triggering cell cycle arrest and the activation of DNA repair genes. This tight coordination between transcription, cell cycle progression, and DNA stress response is crucial for maintaining cellular integrity. Cyclin-dependent kinases CDK7 and CDK9 are central to both transcription and cell cycle regulation. CDK7 functions as the CDK-activating kinase (CAK), essential for activating other CDKs, while CDK9 acts as a critical integrator of signals from both the cell cycle and transcriptional machinery. This review elucidates the mechanisms by which CDK7 and CDK9 regulate the mitotic process and cell cycle checkpoints, emphasizing their roles in balancing cell growth, homeostasis, and DNA repair through transcriptional control.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"962-974"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981567","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

The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts. SGLT2抑制剂canagliflozin可减轻人心脏成纤维细胞高糖诱导的线粒体氧化应激和钙处理的改变。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2024-11-01 Epub Date: 2025-04-21 DOI: 10.1080/15384101.2025.2492423

Fahimeh Varzideh, Urna Kansakar, Scott Wilson, Stanislovas S Jankauskas, Gaetano Santulli

{"title":"The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts.","authors":"Fahimeh Varzideh, Urna Kansakar, Scott Wilson, Stanislovas S Jankauskas, Gaetano Santulli","doi":"10.1080/15384101.2025.2492423","DOIUrl":"10.1080/15384101.2025.2492423","url":null,"abstract":"Cardiac fibrosis and remodeling are critical contributors to heart failure, particularly in the context of diabetes, where hyperglycemia (HG) exacerbates pathological fibroblast activity. Despite the known cardiovascular benefits of canagliflozin (CANA), its specific effects on human cardiac fibroblasts (HCFs) under HG conditions remain unexplored. We investigated whether CANA could mitigate HG-induced detrimental responses in HCFs. Dose-response assays revealed that 100 nM CANA significantly reduced HG-induced proliferation and migration of HCFs. Furthermore, CANA attenuated mitochondrial reactive oxygen species (ROS) production, a key driver of myofibroblast differentiation, and suppressed HG-induced expression of SMAD2, a critical activator of cardiac fibroblasts. Additionally, HG disrupted calcium (Ca2+) homeostasis, which was ameliorated by CANA treatment. These findings collectively demonstrate that CANA exerts protective effects on HCFs by improving mitochondrial function, restoring Ca2+ handling, and reducing fibroblast proliferation, migration, and activation under HG conditions.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"923-930"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986404","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