Research of in vivo reprogramming toward clinical applications in regenerative medicine: A concise review DOI Creative Commons

Yoshihiko Nakatsukasa,

Yosuke Yamada, Yasuhiro Yamada

et al.

Regenerative Therapy, Journal Year: 2024, Volume and Issue: 28, P. 12 - 19

Published: Nov. 27, 2024

Language: Английский

Chemical reprogramming for cell fate manipulation: Methods, applications, and perspectives DOI Creative Commons

Jinlin Wang,

Shicheng Sun, Hongkui Deng

et al.

Cell stem cell, Journal Year: 2023, Volume and Issue: 30(9), P. 1130 - 1147

Published: Aug. 24, 2023

Language: Английский

Citations

47

BayesAge 2.0: a maximum likelihood algorithm to predict transcriptomic age DOI Creative Commons
Lajoyce Mboning, Emma K. Costa, Jingxun Chen

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 3, 2025

Abstract Aging is a complex biological process influenced by various factors, including genetic and environmental influences. In this study, we present BayesAge 2.0, an upgraded version of our maximum likelihood algorithm designed for predicting transcriptomic age (tAge) from RNA-seq data. Building on the original framework, which was developed epigenetic prediction, 2.0 integrates Poisson distribution to model count-based gene expression data employs LOWESS smoothing capture nonlinear gene-age relationships. provides significant improvements over traditional linear models, such as Elastic Net regression. Specifically, it addresses issues bias in predictions, with minimal age-associated observed residuals. Its computational efficiency further distinguishes reference construction cross-validation are completed more quickly compared regression, requires extensive hyperparameter tuning. Overall, represents step forward tAge offering robust, accurate, efficient tool aging research biomarker development.

Language: Английский

Citations

1

Insights and Interventions in Age-Associated Inflammation DOI
Haoyan Huang, Jie Ren, Guang‐Hui Liu

et al.

Current Opinion in Genetics & Development, Journal Year: 2025, Volume and Issue: 91, P. 102306 - 102306

Published: Jan. 20, 2025

Language: Английский

Citations

1

Conserved Biological Processes in Partial Cellular Reprogramming: Relevance to Aging and Rejuvenation DOI
Roberto A. Avelar, Daniel H. Palmer, Anton Kulaga

et al.

Ageing Research Reviews, Journal Year: 2025, Volume and Issue: unknown, P. 102737 - 102737

Published: March 1, 2025

Language: Английский

Citations

0

Decoding human chemical reprogramming: mechanisms and principles DOI
Lin Cheng, Yanglu Wang, Jingyang Guan

et al.

Trends in Biochemical Sciences, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0

Resilience and restoration from fasting-refeeding mediated by a nutrient-regulated linker histone DOI Creative Commons
Kazuto Kawamura,

Anna R. Diederich,

Birgit Gerisch

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 19, 2025

Abstract Intermittent fasting and fasting-refeeding regimens can slow biological aging across taxa 1 . Shifts between fed fasted states activate ancient nutrient-sensing pathways which alter cellular epigenetic to promote longevity 2–4 Yet how age trajectories progress during fasting-refeeding, reprogram state remain largely unknown. Here we observe increases in predicted of Caenorhabditis elegans prolonged adult reproductive diapause, followed by extraordinary reduction refeeding. We identify hil-1 / H1-0 as an evolutionarily conserved nutrient-regulated linker histone mediates adaptations refeeding downstream FOXO TFEB transcription factors. In C. human cell culture, upregulation low-nutrient promotes long-term survival subsequent refeeding-induced recovery. Restoration after is improved enhancing the natural downregulation specifically Our study identifies HIL-1/H1.0 part ancestral switch that reprograms metabolic underlying resilience restoration.

Language: Английский

Citations

0

Unlocking regeneration: how partial reprogramming resembles tissue healing DOI Creative Commons
Melissa T. Adams, Heinrich Jasper, Lluc Mosteiro

et al.

Current Opinion in Genetics & Development, Journal Year: 2025, Volume and Issue: 93, P. 102351 - 102351

Published: May 1, 2025

Partial reprogramming achieved by the transient expression of transcription factors (TFs) Oct4, Sox2, Klf4 and C-Myc (abbreviated OSKM) can erase aging damage features in cells, leading to increased healthspan, lifespan tissue regeneration. Recent reports suggest that mechanisms partial may share some similarities with natural dedifferentiation Both processes appear involve repression somatic identity through sequestration TFs noncanonical sites, which are opened high pioneer TFs, into a fetal-like state. Here, we review reported benefits on regeneration propose common mechanism epigenetic remodeling after injury.

Language: Английский

Citations

0

Manipulating cell fate through reprogramming: approaches and applications DOI

Masaki Yagi,

Joy E. Horng, Konrad Hochedlinger

et al.

Development, Journal Year: 2024, Volume and Issue: 151(19)

Published: Sept. 30, 2024

ABSTRACT Cellular plasticity progressively declines with development and differentiation, yet these processes can be experimentally reversed by reprogramming somatic cells to induced pluripotent stem (iPSCs) using defined transcription factors. Advances in technology over the past 15 years have enabled researchers study diseases patient-specific iPSCs, gain fundamental insights into how cell identity is maintained, recapitulate early stages of embryogenesis various embryo models, reverse aspects aging cultured animals. Here, we review compare currently available approaches, including factor-based methods small molecule-based derive characteristic embryos. Additionally, discuss our current understanding mechanisms that resist their role maintenance. Finally, recent efforts rejuvenate tissues factors, as well application iPSCs deriving novel models pre-implantation development.

Language: Английский

Citations

2

Rewriting cellular fate: epigenetic interventions in obesity and cellular programming DOI Creative Commons
Ruilin Li, Sheng Kang

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: Oct. 10, 2024

External constraints, such as development, disease, and environment, can induce changes in epigenomic patterns that may profoundly impact the health trajectory of fetuses neonates into adulthood, influencing conditions like obesity. Epigenetic modifications encompass processes including DNA methylation, covalent histone modifications, RNA-mediated regulation. Beyond forward cellular differentiation (cell programming), terminally differentiated cells are reverted to a pluripotent or even totipotent state, is, reprogramming. modulators facilitate erase both vivo vitro during programming Noticeably, obesity is complex metabolic disorder driven by genetic environmental factors. Increasing evidence suggests epigenetic play critical role regulation gene expression involved adipogenesis, energy homeostasis, pathways. Hence, we discuss mechanisms which interventions influence obesity, focusing on non-coding RNAs. We also analyze methodologies have been pivotal uncovering these regulations, i.e., Large-scale screening has instrumental identifying genes pathways susceptible control, particularly context adipogenesis homeostasis; Single-cell RNA sequencing (scRNA-seq) provides high-resolution view at individual cell level, revealing heterogeneity dynamics reprogramming; Chromatin immunoprecipitation (ChIP) assays, focused candidate genes, crucial for characterizing transcription factor binding specific genomic loci, thereby elucidating govern programming; Somatic nuclear transfer (SCNT) fusion techniques employed study reprogramming accompanying cloning generation hybrid with characteristics, etc. These approaches marks implicated providing foundation developing targeted therapeutic interventions. Understanding dynamic interplay between advancing mechanism clinical management

Language: Английский

Citations

2

BayesAge 2.0: A Maximum Likelihood Algorithm To Predict Transcriptomic Age DOI Creative Commons
Lajoyce Mboning, Emma K. Costa, Jingxun Chen

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 19, 2024

Abstract Aging is a complex biological process influenced by various factors, including genetic and environmental influences. In this study, we present BayesAge 2.0, an improved version of our maximum likelihood algorithm designed for predicting transcriptomic age (tAge) from RNA-seq data. Building on the original framework, which was developed epigenetic prediction, 2.0 integrates Poisson distribution to model count-based gene expression data employs LOWESS smoothing capture non-linear gene-age relationships. provides significant improvements over traditional linear models, such as Elastic Net regression. Specifically, it addresses issues bias in predictions, with minimal age-associated observed residuals. Its computational efficiency further distinguishes reference construction cross-validation are completed more quickly compared regression, requires extensive hyperparameter tuning. Overall, represents notable advance offering robust, accurate, efficient tool aging research biomarker development.

Language: Английский

Citations

1