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Under homeostatic conditions, balanced M1\/M2 polarization preserves tissue integrity by coordinating immune surveillance, efferocytosis, and tissue repair. When this equilibrium is disrupted, however, M1\u2010skewed responses drive chronic inflammation and autoimmunity, whereas M2\u2010skewed polarization facilitates tumor immune evasion and organ fibrosis. Although diverse therapeutic strategies\u2014including reprogramming, depletion, blockade of monocyte recruitment, CAR\u2010M cells, and nanomedicine\u2014are being explored to restore homeostasis, clinical translation remains constrained by the lack of pathogenic subset\u2010specific markers, insufficient predictive biomarkers for patient stratification, species divergence between mice and humans, and the temporal complexity of context\u2010dependent intervention windows. In this Review, we systematically delineate macrophage plasticity and the molecular mechanisms underlying polarization imbalance, evaluate existing and emerging macrophage\u2010directed interventions, and dissect these translational bottlenecks in depth, highlighting how single\u2010cell multi\u2010omics, humanized models, and dynamic biomarkers can overcome them. 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