{'fraction_non_alphanumeric': 0.04236006051437216, 'fraction_numerical': 0.019667170953101363, 'mean_word_length': 5.895833333333333, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Kidney injury molecule‐1 (KIM‐1)‐mediated anti‐inflammatory activity is preserved by Mucin 1 (MUC1) induction in the proximal tubule during ischemia‐reperfusion injury

. Cell‐associated KIM‐1 exerts an anti‐inflammatory role following kidney injury by mediating apoptotic cell phagocytosis and downregulating the NF‐kB pathway. KIM‐1 cleavage blunts its anti‐inflammatory activities. We reported that MUC1 is protective in a mouse model of ischemia‐reperfusion injury (IRI). As both KIM‐1 and MUC1 are induced in the proximal tubule (PT) during IRI and are ADAM17 substrates, we designed experiments to understand if MUC1 affects KIM‐1 expression and activity.