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Preclinical studies have shown a genetic deletion of antioxidant enzymes (e.g., SOD, GPx) inducing HTN in mice (Carlström et al., 2010), whereas human data led to elevated OS biomarkers (e.g., F2-isoprostanes) preceding HTN onset in normotensive individuals (Rodrigo et al., 2021)

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In short-bowel syndrome escalating throughout 4 weeks, the constant weight gain above preoperative values started immediately with peroral and parental BPC 157 therapy and the villus height, crypth depth and muscle thickness (inner (circular) muscular layer) additionally increased[3]