Journal of Cellular Physiology最新文献

{"title":"Correction to “Beta-Arrestin 2 Mediates Cardiac Hypertrophy Induced by Thyroid Hormones via AT1R”","authors":"","doi":"10.1002/jcp.70030","DOIUrl":"https://doi.org/10.1002/jcp.70030","url":null,"abstract":"<p>Caroline A. L., L. de Bortoli Teixeira, S. C. Simões, et al. 2021. <i>Journal of Cellular Physiology</i> 236, no. 6: 4640–4654.</p><p>In Figure 4B of “Results” section, the images representing GAPDH protein expression in the nucleus and Histone expression in the cytoplasm were inadvertently omitted. The correct images representative Western Blotting images are presented below.</p><p>The authors apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Porphyromonas Gingivalis and Dental Stem Cells Crosstalk Amplify Inflammation and Bone Loss in the Periodontitis Niche","authors":"","doi":"10.1002/jcp.70021","DOIUrl":"https://doi.org/10.1002/jcp.70021","url":null,"abstract":"<p><b>RETRACTION:</b> D. Ezhilarasan, and S. S. Varghese, “Porphyromonas Gingivalis and Dental Stem Cells Crosstalk Amplify Inflammation and Bone Loss in the Periodontitis Niche,” <i>Journal of Cellular Physiology</i> 237, no. 10 (2022): 3768-3777, https://doi.org/10.1002/jcp.30848.</p><p>The above article, published online on 4 August 2022 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. Following publication, it has come to the attention of the journal that the article was accepted solely on the basis of compromised peer review processes. Therefore, the decision to retract this article was taken. The authors have been informed of the decision of retraction and disagree with it.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pleiotropic Role of TNIK in Sepsis-Induced Cardiomyopathy","authors":"Wenwen Yang,&nbsp;Aizhen Zhao,&nbsp;Wangrui Lei,&nbsp;Junmin Chen,&nbsp;Huanle Yan,&nbsp;Jiawen Li,&nbsp;Yang Yang,&nbsp;Ying Chen","doi":"10.1002/jcp.70027","DOIUrl":"https://doi.org/10.1002/jcp.70027","url":null,"abstract":"<div>\u0000 \u0000 <p>Heart failure induced by sepsis is considered one of the foremost contributors to mortality in intensive care unit (ICU) patients. However, the molecular mechanism of myocardial damage in sepsis has not been fully elucidated at present. TNF receptor-associated factor-2 and Nck-interacting protein kinase (TNIK) are members of the germinal center kinase superfamily. TNIK exhibits a pivotal role as a conserved modulator of glucose and lipid homeostasis. Here, we aimed to investigate the potential direct roles of TNIK and whether TNIK exerts anti-septic myocardial damage by regulating the NLRP3 pathway. We initially revealed that TNIK was the crucial involvement of septic myocardial injury. Subsequently, we constructed a cecal ligation and puncture (CLP) mouse model and employed LPS-induced injury in HL-1 cardiomyocytes. Our observations revealed an upregulation of TNIK levels in both CLP-injured mice and LPS-treated HL-1 cells. However, TNIK inhibitor TNIK-IN-7 or siRNA attenuated cardiomyocyte LPS injury. Especially, TNIK siRNA can significantly downregulate TNIK as well as decrease NLRP3 and IL-1β mRNA and protein levels, though the explicit molecular mechanisms of TNIK-NLRP3 in septic myocardial require further investigation. Together, our investigation presents novel evidence suggesting TNIK as a potential therapeutic target for the prevention and therapeutic intervention in sepsis-induced cardiomyopathy.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762222","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}

{"title":"RETRACTION: Phytosomal Curcumin Inhibits Tumor Growth in Colitis-Associated Colorectal Cancer","authors":"","doi":"10.1002/jcp.70018","DOIUrl":"https://doi.org/10.1002/jcp.70018","url":null,"abstract":"<p><b>RETRACTION:</b> R. M. Marjaneh, F. Rahmani, S. M. Hassanian, N. Rezaei, M. Hashemzehi, A. Bahrami, F. Ariakia, H. Fiuji, A. Sahebkar, A. Avan, and M. Khazaei, “Phytosomal Curcumin Inhibits Tumor Growth in Colitis-Associated Colorectal Cancer,” <i>Journal of Cellular Physiology</i> 233, no. 10 (2018): 6785-6798, https://doi.org/10.1002/jcp.26538.</p><p>The above article, published online on 8 May 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.</p><p>The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, evidence of inappropriate post-acquisition image editing, including splicing sites have been detected in Figure 6a. Furthermore, no correspondence between sections at lower and higher magnification was found for the “AOM”, “5-FU”, and “Curcumin” groups in Figure 4e and f. The authors were unable to retrieve the original data underlying the Western Blot experiments presented in Figure 6a due to the time elapsed since performing the experiments. Additionally, original data provided for Figure 4 was insufficient to resolve the issues. Accordingly, the article is retracted as the editors have lost confidence in the accuracy and integrity of the whole body of data presented in the article and consider its conclusions invalid. The authors have been informed of the decision of retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Thromboxane Levels in Ovarian Follicular Fluid Are Inversely Correlated With Oocyte Maturation: Implications of PAR-2/-3 Cooperation and Thromboxane Participation in Follicle Development","authors":"Hsuan-Ting Chen,&nbsp;Tsung-Hsuan Lai,&nbsp;Jun-Jie Lin,&nbsp;Chao-Chi Chen,&nbsp;Wen-Bin Wu","doi":"10.1002/jcp.70025","DOIUrl":"https://doi.org/10.1002/jcp.70025","url":null,"abstract":"<div>\u0000 \u0000 <p>It has been reported the presence of components from the coagulation thrombin-generating pathway and prostaglandins (PGs) in human ovarian follicular fluid (FF) but with unclear functions. Moreover, thrombin can induce COX-2 expression linking to PG synthesis in several cell types. Therefore, this study sought to explore the thromboxane (TX) generation in FF and the correlation between FF TX levels and oocyte maturation. The FF TXB₂ (a stable metabolite of TXA₂) levels exhibited a negative correlation between large preovulatory leading and small mid-antral follicles from in vitro fertilization (IVF) patients, indicating a requirement of TX for a small follicle/oocyte to grow/mature. Further receiver operating characteristic curve analysis identified that intrafollicular TXB₂ level could predict oocyte maturity. Thrombin was found expressed in a similar pattern/trend to TXB₂ in intrafolliclar FF, where it could induce TXB₂ production/secretion in human ovarian follicular GCs via proteinase-activated receptor-2 (PAR-2) and PAR-3 cooperation/transactivation and Erk/p38 MAPK/JNK signaling to cause COX-2/TXB₂ induction. Accordingly, PAR-2 and -3 were present in human ovarian follicular GCs and thrombin, PAR-2 agonist, and TXA₂ analog caused a substantial enhancement in follicle development, which could be blocked by the PAR-2, COX-2, and TXA₂ prostanoid (TP) receptor inhibitors in an ex vivo cultured murine ovary model. Collectively, we first demonstrated that FF thrombin regulates PAR-2/-3 cooperation and MAPK signaling pathways to induce COX-2 expression and TX production in follicular GCs, possibly supporting intrafollicular TX levels and triggering TP-related pathways to enhance follicle development. The FF TX levels also can be a predictor for oocyte maturation during IVF.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749439","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}

{"title":"SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy","authors":"Juan J. Ferreira,&nbsp;Lindsey N. Kent,&nbsp;Ronald McCarthy,&nbsp;Alice Butler,&nbsp;Xiaofeng Ma,&nbsp;Nikita Peramsetty,&nbsp;Chinwendu Amazu,&nbsp;Alexander Zhang,&nbsp;Grace C. Whitter,&nbsp;Ethan Li,&nbsp;Sarah K. England,&nbsp;Celia M. Santi","doi":"10.1002/jcp.70024","DOIUrl":"https://doi.org/10.1002/jcp.70024","url":null,"abstract":"<p>At the end of pregnancy, the uterus transitions from a quiescent to a highly contractile state. This is partly due to the depolarization of the resting membrane potential in uterine (myometrial) smooth muscle cells (MSMCs). In human MSMCs, the membrane potential is regulated by a functional complex between the sodium (Na⁺)-activated potassium (K⁺) channel SLO2.1 and the Na⁺ leak channel nonselective (NALCN). Na⁺ entering through NALCN activates SLO2.1, leading to K⁺ efflux, membrane hyperpolarization (cells become more negative inside), and reduced contractility. Decreased SLO2.1/NALCN activity results in reduced K⁺ efflux, leading to membrane depolarization, Ca²⁺ influx via voltage-dependent calcium channels, and increased MSMC contractility. However, all of these data are from MSMCs isolated from women at term, so the role of the SLO2.1/NALCN complex early in pregnancy was speculative. To address this question here, we examined the role of the SLO2.1/NALCN complex in regulating mouse MSMC membrane potential across pregnancy. We report that <i>Slo2.1</i> and <i>Nalcn</i> are more highly expressed in MSMCs from nonpregnant and early pregnant mice than in those from late-pregnant mice. Functional studies revealed that SLO2.1 channels mediate a significant portion of the K⁺ current in mouse MSMCs, particularly in cells from nonpregnant and early pregnant mice. Activation of SLO2.1 by Na⁺ influx through NALCN led to membrane hyperpolarization in MSMCs from early pregnancy but not in MSMCs from later pregnancy. Moreover, the NALCN/SLO2.1 complex regulates intracellular Ca²⁺ responses more in MSMCs from nonpregnant and early pregnancy mice than in MSMCs from late pregnancy. Together, these findings reveal that the SLO2.1/NALCN functional complex is conserved between mice and humans and functions throughout pregnancy. This study could open avenues for targeted pharmacological interventions for pregnancy-related complications.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: DUSP1 Recuses Diabetic Nephropathy via Repressing JNK-Mff-Mitochondrial Fission Pathways","authors":"","doi":"10.1002/jcp.70017","DOIUrl":"https://doi.org/10.1002/jcp.70017","url":null,"abstract":"<p><b>RETRACTION:</b> Sheng, J., H. Li, Q. Dai, C. Lu, M. Xu, J. Zhang, and J. Feng, “DUSP1 Recuses Diabetic Nephropathy via Repressing JNK-Mff-Mitochondrial Fission Pathways.” <i>Journal of Cellular Physiology</i> 234, no. 3 (2019): 3043-3057. https://doi.org/10.1002/jcp.27124.</p><p>The above article, published online on September 7, 2018, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Several irregularities were found, including, but not limited to, multiple image elements being published in later articles by different author groups and in distinct scientific contexts, indicating inappropriate data sharing. The authors were invited to comment on these concerns but did not respond. Further investigation by the publisher revealed that the article was accepted solely on the basis of a compromised peer review process. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SMC2 and Condensin II Subunits Are Essential for the Development of Hematopoietic Stem and Progenitor Cells in Zebrafish","authors":"Chang-Kyu Oh,&nbsp;Man S. Kim,&nbsp;Unbeom Shin,&nbsp;Ji Wan Kang,&nbsp;Yun Hak Kim,&nbsp;Hwa Soo Ko,&nbsp;Jae Sun Ra,&nbsp;Soyul Ahn,&nbsp;Eun Young Choi,&nbsp;Sanghyeon Yu,&nbsp;Uijeong Nam,&nbsp;Taesoo Choi,&nbsp;Kyungjae Myung,&nbsp;Yoonsung Lee","doi":"10.1002/jcp.70023","DOIUrl":"https://doi.org/10.1002/jcp.70023","url":null,"abstract":"<p>Hematopoietic stem and progenitor cells (HSPCs) play a pivotal role in blood cell production, maintaining the health and homeostasis of individuals. Dysregulation of HSPC function can lead to blood-related diseases, including cancer. Despite its importance, our understanding of the genes and pathways underlying HSPC development and the associated pathological mechanisms remains limited. To elucidate these unknown mechanisms, we analyzed databases of patients with blood disorders and performed functional gene studies using zebrafish. We employed bioinformatics tools to explore three public databases focusing on patients with myelodysplastic syndrome (MDS) and related model studies. This analysis identified significant alterations in several genes, especially <i>SMC2</i> and other condensin-related genes, in patients with MDS. To further investigate the role of Smc2 in hematopoiesis, we generated <i>smc2</i> loss-of-function zebrafish mutants using CRISPR mutagenesis. Further analyses of the mutants revealed that <i>smc2</i> depletion induced G2/M cell cycle arrest in HSPCs, leading to their maintenance and expansion failure. Notably, although the condensin II subunits (<i>ncaph2</i>, <i>ncapg2</i>, and <i>ncapd3</i>) were essential for HSPC maintenance, the condensin I subunits did not affect HSPC development. These findings emphasize the crucial role of condensin II in ensuring healthy hematopoiesis via promoting HSPC proliferation.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiomyocytic FoxP3 Attenuates Expression of β Isoform of Myosin Heavy Chain During Cardiac Hypertrophy and Effects of Triptolide","authors":"Jia-Hui Hong,&nbsp;Xi-Chun Pan,&nbsp;Ya-Lan Xiong,&nbsp;Peng Wang,&nbsp;Yao Yuan,&nbsp;Ya Liu,&nbsp;Hai-Gang Zhang","doi":"10.1002/jcp.70026","DOIUrl":"https://doi.org/10.1002/jcp.70026","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiac hypertrophy, a maladaptive response to chronic stress, progresses to heart failure through mechanisms requiring deeper exploration. While forkhead helix transcription factor P3 (FoxP3) is well-known as a key regulator in CD4⁺ T cells, its role in cardiomyocytes remains unclear. Here, by using isoproterenol (ISO)-induced cardiac hypertrophy models (40 mg/kg daily for in vivo study and 10 μmol/L for in vitro study), we revealed the protective role of FoxP3 in cardiac hypertrophy. Though modulating FoxP3 expression using siRNA or plasmid in cardiomyocytes, we found that FoxP3 knockdown exacerbated ISO-induced hypertrophic responses, while overexpression of FoxP3 attenuated hypertrophic effects. The protective function of cardiomyocytic FoxP3 in vivo was further confirmed by infection of adeno-associated virus. Mechanically, the cardiomyocytic FoxP3 decreased the expression of nuclear factor of activated T cells c3 (NFATc3), a key regulator of hypertrophy-related genes, to suppress hypertrophy-related genes, including atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain (β-MHC), and thus ameliorate hypertrophic responses. Besides, the immunoprecipitation and immunofluorescence determination showed that FoxP3 could interact with NFATc3 in the nucleus to form a transcription complex, thereby regulating the transcription activity of NFATc3. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assays (EMSAs) revealed the specific binding sequences of FoxP3 in the β-MHC promoter region, with binding occupancy reduced by ISO, suggesting that FoxP3 could interact with NFATc3 to down-regulate the β-MHC expression. Importantly, we identified triptolide (TP), a bioactive natural product, as a potent inducer of FoxP3 expression. Both in vivo (10 μg/kg daily) and in vitro (10 μmol/L) studies demonstrated that TP significantly reversed cardiac hypertrophy by upregulating FoxP3 expression, thereby inhibiting NFATc3-mediated β-MHC transcription. These findings highlight cardiomyocytic FoxP3 as a novel protective factor, elucidating its underlying mechanisms and demonstrating the therapeutic potential of TP in this process.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690123","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}

{"title":"Daytime-Restricted Feeding Alleviates D-Galactose-Induced Aging in Mice and Regulates the AMPK and mTORC1 Activities","authors":"Tiepeng Li,&nbsp;Ning Huang,&nbsp;Honghan Chen,&nbsp;Yu Yang,&nbsp;Jian Zhang,&nbsp;Weitong Xu,&nbsp;Hui Gong,&nbsp;Chuhui Gong,&nbsp;Ming Yang,&nbsp;Tingting Zhao,&nbsp;Fangfang Wang,&nbsp;Hengyi Xiao","doi":"10.1002/jcp.70020","DOIUrl":"https://doi.org/10.1002/jcp.70020","url":null,"abstract":"<div>\u0000 \u0000 <p>Time-restricted feeding (TRF) is a distinct regimen of intermittent fasting advocated for health improving. Although nighttime TRF (NRF) in rodents is analogous to daytime TRF (DRF) in humans and has health benefits, the effects of DRF on rodent's health remain uncertain. The adverse health effects of DRF in rodents are primarily attributed to its implementation-induced temporal shift in the expression of circadian rhythm-related genes. However, studies also demonstrate the health–beneficial effect of restricted feeding itself on metabolic homeostasis, particularly in periphery tissues. Moreover, the direct effects of DRF on aging progression in rodents are underexplored, highlighting a gap in current research. To explore the overall health effects of long-term DRF in rodents, especially its influence on aging progression, we investigated the impact of long-term DRF on mice under a progeric aging condition. Results showed that both 4-h and 8-h DRF regimens exerted positive effects on aging retardation; these effects were manifested as improved physical and memory capacities, enhanced liver and kidney functions, and reduced oxidative damage and inflammatory response. These DRF regimens also lowered the manifestation of aging-related markers in peripheral tissues, with decreased SA-β-gal staining and p16 expression. Mechanistically, DRF regimens, especially DRF8, upregulated AMPK signaling and downregulated mTORC1 signaling. Interestingly, the health benefits of DRF are similar to those of metformin intervention. In conclusion, our study demonstrates for the first time that DRF effectively counteracts oxidative stress-induced aging progression in mice, supporting the viewpoint that TRF as a promising strategy for preventing aging and aging-related disorders.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595032","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}