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Metabolism has been implicated in cell fate determination, particularly through epigenetic modifications. Similarly, lipid remodeling also plays a role in regulating cell fate. Here, we present comprehensive lipidomics analysis during BMP4-driven primed to naive pluripotency transition or BiPNT and demonstrate that lipid remodeling plays an essential role. We further identify Cpt1a as a rate-limiting factor in BiPNT, driving lipid remodeling and metabolic reprogramming while simultaneously increasing intracellular acetyl-CoA levels and enhancing H3K27ac at chromatin open sites. Perturbation of BiPNT by histone acetylation inhibitors suppresses lipid remodeling and pluripotency transition. Together, our study suggests that lipid remodeling promotes pluripotency transitions and further regulates cell fate decisions, implicating Cpt1a as a critical regulator between primed-naive cell fate control.
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http://dx.doi.org/10.1038/s42003-024-06874-3 | DOI Listing |
Nat Aging
September 2025
Aging Biomarker Consortium (ABC), Beijing, China.
The global surge in the population of people 60 years and older, including that in China, challenges healthcare systems with rising age-related diseases. To address this demographic change, the Aging Biomarker Consortium (ABC) has launched the X-Age Project to develop a comprehensive aging evaluation system tailored to the Chinese population. Our goal is to identify robust biomarkers and construct composite aging clocks that capture biological age, defined as an individual's physiological and molecular state, across diverse Chinese cohorts.
View Article and Find Full Text PDFMar Environ Res
September 2025
Key Laboratory of Marine Ecology and Environmental Sciences, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, PR China; Laboratory for Marine Ecology and Environmental Science, Qingdao Marine Science and Technology Center, Qingdao, 266237, PR China; University of Chinese Academ
Phosphorus (P) is a critical limiting nutrient for phytoplankton growth in aquatic ecosystems. Under P-limitation, phytoplankton adapt by remodeling membrane lipids, replacing phospholipids (PLs) with non-P lipids such as sulfolipid sulfoquinovosyldiacylglycerol (SQDG) and betaine lipids (BLs). This mechanism is essential for reevaluating the relationship between phosphate (PO) concentrations and primary productivity.
View Article and Find Full Text PDFZool Res
September 2025
State Key Laboratory of Agricultural Products Safety, Ningbo University, Ningbo, Zhejiang 315211, China.
Apoptosis preserves organismal homeostasis by selectively eliminating unnecessary or damaged cells, with accumulating evidence also suggesting that it activates regenerative pathways and facilitates tissue remodeling. To date, however, the regulatory mechanisms linking this form of programmed cell death to regeneration remain poorly defined, particularly in evolutionarily basal organisms. Using the sea cucumber ( ) as a model for intestinal regeneration, this study identified robust apoptotic activity across key regenerative stages.
View Article and Find Full Text PDFFront Oncol
August 2025
The First Clinical School of Nanjing University of Chinese Medicine, Nanjing, China.
Ferroptosis is a regulated, non-apoptotic form of cell death marked by the accumulation of iron-dependent lipid peroxides. This process causes rapid rupture of the plasma membrane and the release of intracellular contents. Ferroptosis acts as an intrinsic tumor-suppressive mechanism.
View Article and Find Full Text PDFFerroptosis, an iron-dependent cell death pathway driven by lipid peroxidation, has emerged as a critical pathophysiological mechanism linking cancer and inflammatory diseases. The seemingly distinct pathologies exhibit shared microenvironmental hallmarks-oxidative stress, immune dysregulation, and metabolic reprogramming-that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor-suppressive mechanism and a driver of inflammatory tissue damage.
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