CXCR4 is expressed on leukaemia cells and haematopoietic stem cells (HSCs), and its ligand stromal‐derived factor 1 (SDF‐1) is produced abundantly by stromal cells in the bone marrow (BM). The SDF‐1/CXCR4 axis plays important roles in homing to and retention in the protective BM microenvironment of malignant leukaemia cells and normal HSCs. CXCR4 expression is regulated by multiple mechanisms and the level of CXCR4 expression on leukaemia cells has prognostic indications in patients with acute leukaemia. CXCR4 antagonists can mobilize leukaemia cells from BM to circulation, which render them effectively eradicated by chemotherapeutic agents, small molecular inhibitors or hypomethylating agents. Therefore, such combinational therapies have been tested in clinical trials. However, new evidence emerged that drug‐resistant leukaemia cells were not affected by CXCR4 antagonists, and the migration of certain leukaemia cells to the leukaemia niche was independent of SDF‐1/CXCR4 axis. In this review, we summarize the role of CXCR4 in progression and treatment of acute leukaemia, with a focus on the potential of CXCR4 as a therapeutic target for acute leukaemia. We also discuss the potential value of using CXCR4 antagonists as chemosensitizer for conditioning regimens and immunosensitizer for graft‐vs‐leukaemia effects of allogeneic haematopoietic stem cell transplantation.

Aging is an extremely intricate and progressive phenomenon that is implicated in many physiological and pathological conditions. Icariin (ICA) is the main active ingredient of Epimedium and has exhibited multiple bioactivities, such as anti‐tumor, neuroprotective, antioxidant, anti‐inflammatory, and anti‐aging properties. ICA could extend healthspan in both invertebrate and vertebrate models. In this review, the roles of ICA in protection from declined reproductive function, neurodegeneration, osteoporosis, aging intestinal microecology, and senescence of cardiovascular system will be summarized. Furthermore, the underlying mechanisms of ICA‐mediated anti‐aging effects will be introduced. Finally, we will discuss some key aspects that constrain the usage of ICA in clinical practice and the corresponding strategies to solve these issues.

Luteolin, a natural flavonoid, exerts broad immunomodulatory effects across multiple immune cell populations, positioning it as a promising candidate for treating inflammatory diseases, infections, and cancer. This review synthesizes current evidence on luteolin’s effects on T cells, natural killer (NK) cells, dendritic cells (DCs), macrophages, neutrophils, eosinophils, and basophils. Luteolin promotes the differentiation of regulatory T cells (Tregs) and suppresses pro-inflammatory T helper 17 (Th17) and Th2 responses, thereby restoring immune balance in sepsis, allergies, and autoimmunity. In macrophages, it skews polarization toward the anti-inflammatory M2 phenotype via the signal transducer and activator of transcription 3 (STAT3)/STAT6 and peroxisome proliferator-activated receptor γ (PPARγ) pathways, while inhibiting nuclear factor-κB (NF-κB) and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation. Neutrophil functions are dampened by reduced oxidative stress, adhesion molecule expression, and induction of apoptosis. Luteolin may enhance NK-cell cytotoxicity and DC-mediated antigen presentation while curbing eosinophil and basophil activation in allergic disorders. Despite preclinical successes, future research should prioritize mechanistic insights, structural optimization, and clinical translation to unlock luteolin’s full therapeutic potential.