Significados de renal ir en inglés

Results showed that Tisp40 deficiency attenuates neutrophil and macrophage infiltration after renal IR.

Therefore, CTS could be a useful therapeutic agent in the fight against renal IR injury.

For renal IR, bilateral renal pedicels were exposed and clamped to induce 30 min of ischemia.

However, the role of Tisp40 in renal inflammatory responses and tubular cell proliferation during renal IR injury remains unknown.

In the present study, we investigated the effects of CTS on renal IR injury and its potential underlying mechanisms.

In our previous studies, we demonstrated that Tisp40 exacerbates tubular cell apoptosis and tubulointerstitial fibrosis after renal IR injury.

Our previous studies showed that cyclic helix B peptide (CHBP) improved renal IR-related injury, but its underlying mechanism is not well defined.

Renal IR injury was induced by clamping the bilateral renal artery for 30 minutes followed by 24 hours of reperfusion.