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Fibromodulin deficient mice (Fmod-null) have altered tendons (mechanically weaker and morphologically altered) that exhibit increased LOX-induced mature crosslinks within collagen type I C-telopeptide domains, but LOX itself does not appear to be affected through post-translational modifications (Kalamajski et al ., 2014)

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Strategies targeting metabolic vulnerabilities will not only eliminate backup systems to prevent ferroptosis [49] , but also receive considerable attention in cancer therapeutics [54]