Core Viewpoint - The article discusses the significant role of periosteal stem cells in bone fracture repair, highlighting their unique properties and the mechanisms behind their activation during injury [5][11]. Group 1: Bone Healing Mechanisms - Bone healing typically follows a process reminiscent of embryonic cartilage development, but the cellular basis and regulatory mechanisms of normal and impaired healing remain unclear [3]. - Periosteal stem cells are crucial for bone development and homeostasis, yet they exhibit high heterogeneity in function and location within different microenvironments [4]. Group 2: Research Findings - A study published in Cell Research identified a specific group of resting periosteal stem cells expressing Angptl7, which are primarily responsible for fracture repair through endochondral ossification [5]. - The research revealed that Angptl7+ cells do not contribute to bone formation under normal conditions but become activated during fracture healing, indicating a specialized role in tissue repair [10]. Group 3: Cellular Heterogeneity - The study utilized single-cell transcriptome sequencing to uncover the heterogeneity of periosteal stem cells, identifying two distinct subpopulations: one expressing Angptl7 and another expressing Postn, with different roles in bone maintenance and repair [8][9]. - Angptl7 cells are associated with stem cell maintenance, while Postn cells are linked to osteogenic differentiation and bone formation [8]. Group 4: Implications for Future Research - The findings provide insights into the cellular basis of efficient bone repair and propose a novel model of tissue repair involving resident stem cells dedicated to injury response [5][11]. - The research establishes a specific lineage tracing mouse model for periosteal cells, which can aid in exploring the molecular mechanisms behind impaired fracture healing and developing new therapeutic strategies [11].

Core Viewpoint - The article discusses the recent announcement of the 2024 Annual Outstanding Paper Awards by Sanofi-Cell Research, highlighting three significant research papers published in Cell Research that have made notable contributions to their respective fields [2]. Group 1: Paper Summaries - The first paper titled "Hypoxia induces mitochondrial protein lactylation to limit oxidative phosphorylation" reveals that hypoxia-induced mitochondrial protein lactylation inhibits oxidative phosphorylation (OXPHOS). The study identifies AARS2 as a lactyltransferase that modifies PDHA1 and CPT2, reducing acetyl-CoA influx and suppressing OXPHOS. SIRT3 can reverse this lactylation, emphasizing the role of lactylation in mitochondrial function regulation [8][13]. - The second paper titled "40 Hz light flickering promotes sleep through cortical adenosine signaling" demonstrates that 40 Hz light flickering increases extracellular adenosine levels in the primary visual cortex via ENT2-mediated transport. The study shows that 30 minutes of 40 Hz light flickering enhances both non-rapid eye movement and rapid eye movement sleep in mice, suggesting a non-invasive strategy for treating insomnia [14][16]. - The third paper discusses a novel design strategy for D-type proteins that can stably target natural L-type proteins or peptides. This research achieves the precise design of enantiomeric protein complexes with high stereospecificity and target specificity, exhibiting significant thermal stability and proteolytic resistance. The findings provide a new platform for disease treatment and biotechnological applications [18].