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We began with the presumption that the reducing potential of cytoplasmic thiol redox components was required to prevent disulfide bonds from forming

Ju J, Zhang H, Lin M, Yan Z, An L, Cao Z, Geng D, Yue J, Tang Y, Tian L et al

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Recently, our approach was the BPC 157 therapy effect (for review see, i.e., [ 2 4 ]) in the study of the permanent occlusion of major vessels-induced occlusion syndromes [ 14 20 ], the occlusion-like syndrome induced by severe intoxication (alcohol, lithium) [ 21 , 22 ] or maintained severe intra-abdominal hypertension [ 23 ] recovered with the activation of the collateral pathways [ 14 23 ]