Increased Elmo1 Expression worsens the AKI-CKD transition via ROS

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and a key contributor to the progression toward chronic kidney disease (CKD), with oxidative stress playing a central role in this transition. Engulfment and Cell Motility 1 (ELMO1) regulates cytoskeletal remodeling and reactive oxygen species (ROS) production through RAC1 activation, yet its involvement in redox imbalance and kidney injury remains unclear. To investigate this, a unilateral renal IRI model was established in wild-type (WT) and ELMO1-overexpressing (Elmo1 H/H) mice. Renal function was evaluated using plasma cystatin C, estimated glomerular filtration rate (eGFR), and urinary albumin-to-creatinine ratio (UACR), while structural and ultrastructural kidney changes were assessed by Masson's trichrome staining and electron microscopy. Redox-related gene expression was analyzed via RT-qPCR, and global transcriptional alterations were examined using RNA sequencing. Overall design: a unilateral renal IRI model was established in wild-type (WT) and ELMO1-overexpressing (Elmo1 H/H) mice.