Hematopoietic Stem Cells (HSCs) rely on complex metabolic and epigenetic regulatory networks to preserve their function. Due to the scarcity of HSCs, technical challenges have limited our insights into the interplay between HSC metabolism and their transcriptional and epigenetic regulation. We recently have established new low-input multi-layer OMICs methods to address the metabolic, lipid and epigenetic profiles of mouse and human HSCs and their downstream progenitors, upon aging and leukemia (Sch\u00f6nberger*, Obier* et al., Cell Stem Cell 2022; Lalioti*, Romero-Mulero* et al., revisions). Mechanistically, we uncover a non-classical retinoic acid signaling axis that regulates HSC identity. Our findings emphasize how a single metabolite controls stem cell fate by instructing epigenetic and transcriptional attributes. Now, we have used these knowledge to in vivo modulate HSC activity upon myocardial infraction, thus emergency hematopoiesis, to improve the heart function (Rettkowski*, Romero-Mulero* et al., Nature Cell Biology 2025, accepted). Further, we have recently shown that GPRC5C is a regulator of human HSC dormancy (Zhang et al., Nature Cell Biology 2022). High GPRC5C levels in AML correlate with poor survival and promote leukemia aggression via NF-\u03baB activation and increased branched-chain amino acids (BCAAs; Zhang et al., Blood Advances 2023). Our findings suggest the GPRC5C-NF-\u03baB-SLC7A5-BCAA axis as a therapeutic target in leukemia.<\/p>\n
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