
-   EGR2 was significantly elevated in myelin-reactive CD4+ T cells from patients with multiple sclerosis and mice with autoimmune neuroinflammation. EGR2 enhanced TH17 cell differentiation and myeloid cell recruitment to the central nervous system (CNS) by upregulating pathogenesis-associated genes and myelomonocytic chemokines. T cell-specific deletion of Egr2 attenuated neuroinflammation without compromising the host's ability to control infections [PMID: 37443284].
-   EGR2 plays a key role in the PTEN-induced apoptotic pathway. EGR2 could induce apoptosis in a large proportion of cancer cell lines by altering the permeability of mitochondrial membranes, releasing cytochrome c and activating caspase-3, -8, and -9. EGR2 directly transactivates expression of BNIP3L and BAK [PMID: 12687019]. Expression of EGR2 was decreased in ovarian tumors compared with corresponding normal tissues. Colony-formation assays indicated that EGR2 was able to suppress growth of cancer cells and knockdown of EGR2 accelerated cell growth [PMID: 11494141].
-   EGR2 expression is a selective property of alveolar macrophages in the lung. EGR2 is driven by TGF-beta and GM-CSF in a PPAR-gamma-dependent manner to control alveolar macrophage differentiation. EGR2 is required for repopulation of the alveolar niche after sterile, bleomycin-induced lung injury and demonstrate that EGR2-dependent, monocyte-derived alveolar macrophages are vital for effective tissue repair after injury [PMID: 34797692].
-   Decreased expression of Egr2 (KROX20) was observed in aortic valves of patients with defective aortic valves (AoVs) disease. Krox20 knockout mice had features of human AoV disease, including excess of proteoglycan deposition and reduction of collagen fibers. Loss of Krox20 results in aortic valve regurgitation and impaired transcriptional activation of fibrillar collagen genes. Krox20-mediated activation of fibrillar Col1a1 and Col3a1 genes is crucial to avoid postnatal degeneration of the AoV leaflets [PMID: 25344368].
-   Transcription factors Early Growth Response 2 (EGR2) was highly induced in tumour infiltrating T cells (TILs) in tumors from cohorts of colorectal, liver and lung cancer patients. Deficiency of Egr2 and 3 in T cells resulted in enhanced tumour growth and fewer TILs in mouse models. Thus, Egr2 is important for maintaining anti-tumour responses of exhausted CD8 + TILs [PMID: 36342511].

## Summary

EGR2 encodes a zinc finger transcription factor involved in various cellular processes including Schwann cell myelination and hindbrain segmentation [CS: 10]. EGR2 regulates gene expression related to cell differentiation, myelin formation, and apoptosis, often in response to tissue damage or inflammation [CS: 10]. This protein's activity includes the direct transactivation of genes such as BNIP3L and BAK, which are involved in the apoptotic pathway by mediating mitochondrial membrane permeability and caspase activation [CS: 8]. In the context of acute kidney injury, the upregulation of EGR2 may reflect a similar protective role in response to cellular stress, activating genes that could promote cell survival pathways or contribute to the repair and regeneration of kidney tissue [CS: 5]. For instance, the mitochondrial role of EGR2 could serve to counteract stress-induced apoptotic signaling in AKI, thereby reducing cell death and preserving renal function [CS: 4].

In acute kidney injury, the inflammatory response is crucial in disease progression [CS: 10]. Elevated EGR2 expression in myelin-reactive CD4+ T cells and its role in enhancing TH17 cell differentiation suggest that in the kidney, EGR2 may modulate the inflammatory milieu [CS: 6]. Upregulation of EGR2 could influence the expression of chemokines, facilitating myeloid cell recruitment to sites of injury for tissue repair and inflammation resolution [CS: 5].
