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Experimental observations suggest that it participates in coordinated cellular repair processes by influencing fibroblast activity, modulating angiogenic signaling, and regulating the expression of structural extracellular matrix components such as collagen and elastin

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Notably, breast cancer cells achieve metabolic adaptation by hijacking the autophagy mechanism: under glucose-deprivation conditions, MANF-mediated mitophagy eliminates dysfunctional mitochondria through the PRKN/Parkin-dependent pathway, maintains the ATP supply and promotes tumour survival [112], suggesting that targeting the MANFPRKN interaction can break the drug resistance barrier of breast cancer under metabolic stress

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doi:10.1176/appi.ajp.163.1.28CrossRefGoogle ScholarPubMed Veronese, N., Stubbs, B., Solmi, M., Ajnakina, O., Carvalho, A