From Bench to Bedside: Translating Cellular Rejuvenation Therapies into Clinical Applications

被引:0
作者
Saliev, Timur [1 ]
Singh, Prim B. [2 ]
机构
[1] SD Asfendiyarov Kazakh Natl Med Univ, Tole Bi St 94, Alma Ata 050000, Kazakhstan
[2] Nazarbayev Univ, Sch Med, Astana 010000, Kazakhstan
关键词
rejuvenation; senolytics; CRISPR; induced pluripotent stem cells; mesenchymal stem cells; ARTIFICIAL-INTELLIGENCE; INFLAMMATION; SENESCENCE; AGE;
D O I
10.3390/cells13242052
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cellular rejuvenation therapies represent a transformative frontier in addressing age-related decline and extending human health span. By targeting fundamental hallmarks of aging-such as genomic instability, epigenetic alterations, mitochondrial dysfunction, and cellular senescence-these therapies aim to restore youthful functionality to cells and tissues, offering new hope for treating degenerative diseases. Recent advancements have showcased a range of strategies, including epigenetic reprogramming, senolytic interventions, mitochondrial restoration, stem cell-based approaches, and gene-editing technologies like CRISPR. Each modality has demonstrated substantial potential in preclinical models and is now being cautiously explored in early-stage clinical trials. However, translating these therapies from the laboratory to clinical practice presents unique challenges: safety concerns, delivery precision, complex regulatory requirements, ethical considerations, and high costs impede widespread adoption. This review examines the current landscape of cellular rejuvenation, highlighting key advancements, potential risks, and the strategies needed to overcome these hurdles.
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页数:24
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[51]  
Zhang K.H., Li Q.L., Zhang Y.X., Nuerlan G., Li Y.Y., Mao J., Gong S.Q., Targeting Mitophagy as a Potential Therapeutic Approach for Age-Related Bone Diseases, Adv. Ther, 7, (2024)
[52]  
Qi X.M., Qiao Y.B., Zhang Y.L., Wang A.C., Ren J.H., Wei H.Z., Li Q.S., PGC-1α/NRF1-dependent cardiac mitochondrial biogenesis: A druggable pathway of calycosin against triptolide cardiotoxicity, Food Chem. Toxicol, 171, (2023)
[53]  
Nandan P.K., Job A.T., Ramasamy T., DRP1 Association in Inflammation and Metastasis: A Review, Curr. Drug Targets, 25, pp. 909-918, (2024)
[54]  
Alghamdi A., A detailed review of pharmacology of MFN1 (mitofusion-1)-mediated mitochondrial dynamics: Implications for cellular health and diseases, Saudi Pharm. J, 32, (2024)
[55]  
Goldman A., Mullokandov M., Zaltsman Y., Regev L., Levin-Zaidman S., Gross A., MTCH2 cooperates with MFN2 and lysophosphatidic acid synthesis to sustain mitochondrial fusion, EMBO Rep, 25, pp. 45-67, (2024)
[56]  
Ribaudo G., Gianoncelli A., An Updated Overview on the Role of Small Molecules and Natural Compounds in the “Young Science” of Rejuvenation, Antioxidants, 12, (2023)
[57]  
Palomera-Avalos V., Grinan-Ferre C., Izquierdo V., Camins A., Sanfeliu C., Pallas M., Metabolic Stress Induces Cognitive Disturbances and Inflammation in Aged Mice: Protective Role of Resveratrol, Rejuvenation Res, 20, pp. 202-217, (2017)
[58]  
Lee J.S., Kim J.R., Byeon E., Kim D.H., Kim H.S., Lee J.S., Molecular Events in Response to Triclosan-Induced Oxidative Stress in CRISPR/Cas9-Mediated-Targeted Mutants in Daphnia magna, Environ. Sci. Technol, 58, pp. 16738-16749, (2024)
[59]  
Liu M., Fu X.Y., Yi Q.H., Xu E.H., Dong L.B., Impaired mitochondrial oxidative phosphorylation induces CD8+T cell exhaustion, Biochem. Biophys. Res. Commun, 734, (2024)
[60]  
Zhou H., Ji Y.J., Li J.J., Sun L., The study on the role of O-GlcNAcylation of SIRT3 in regulating mitochondrial oxidative stress during simulate myocardial ischemia-reperfusion, Sci. Rep, 14, (2024)