The aim of this review is to analyse contemporary scientific evidence concerning the role and significance of macrophage polarisation in the pathogenesis of endometriosis. Particular emphasis is placed on the molecular and cellular mechanisms that regulate macrophage phenotypic differentiation and on how these cells sustain inflammation, angiogenesis, fibrosis and immune tolerance within the peritoneal cavity. Promising research avenues for identifying potential targets that could underpin novel diagnostic approaches and innovative targeted therapies for endometriosis are also examined. A comprehensive search was conducted in PubMed, Scopus, Web of Science and Google Scholar, and 93 in-vitro, in-vivo and clinical studies were included in the final analysis. Peritoneal fluid from patients is characterised by the accumulation of haemolytic iron, heightened oxidative stress and oestrogen-dependent hypersecretion of IL-6, IL-8 and CCL-2, which collectively drive macrophages towards a pro-angiogenic M2 phenotype. M2 macrophages secrete VEGF-A, TGF-β1, MMP-2/-9, IL-10 and neurotrophic factors, thereby exacerbating angiofibrogenesis, promoting neuro-vascular invasion and suppressing clearance of ectopic endometrium via the CD47-SIRPα pathway. Exosomes released by stromal cells of ectopic lesions, enriched with miR-301a-3p, LGMNP1 and lncRNA CHL1-AS1, activate the PI3K/AKT, STAT3 and TGF-β/Smad cascades, further reinforcing M2 polarisation, while metabolic reprogramming (the lactate-METTL3-Trib1 axis and succinate accumulation) coupled with reduced HO-1 expression sustains chronic inflammation. Pre-clinical data indicate that macrophage reprogramming using niclosamide, mifepristone, engineered extracellular vesicles, OMV-based nanoparticles or inhibitors of the lactate-METTL3-Trib1 pathway attenuates lesion volume and alleviates pain. The most promising strategy appears to be combined therapy with autologous M1 macrophages and a mifepristone nanocarrier, which displays synergistic efficacy. Consequently, peritoneal macrophage polarisation constitutes a pivotal element of endometriosis pathogenesis; its targeted modulation represents an innovative, pathogenetically grounded approach that could enhance treatment efficacy and reduce recurrence rates, although further experimental and clinical studies are required for successful clinical translation.