Open Access

REVIEW

Transcriptional factor RUNX1: A potential therapeutic target for fibrotic pulmonary disease

by JIA LIU^1,2,#, FAPING WANG^1,2,#, BO YUAN³, FENGMING LUO^1,2,*

1 Department of Pulmonary and Critical Care Medicine, West China Hospital, Sichuan University, Chengdu, 610041, China
2 Laboratory of Pulmonary Immunology and Inflammation, Department of Respiratory and Critical Care Medicine, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, Chengdu, 610041, China
3 International Medical Center, General Practice Unit, West China Hospital, Sichuan University, Chengdu, 610041, China

* Corresponding Author: FENGMING LUO. Email:
# These authors contributed equally to this article

(This article belongs to the Special Issue: Bioinformatics Study of Diseases)

BIOCELL 2023, 47(4), 697-705. https://doi.org/10.32604/biocell.2023.026148

Received 19 August 2022; Accepted 25 November 2022; Issue published 08 March 2023

Abstract

Runt-related transcription factor-1 (RUNX1), also known as the core-binding factor alpha 2 subunit, is closely related to human leukemia. The functions of RUNX1 in modulating cell proliferation, differentiation, and survival in multiple systems have been gradually discovered with the emergence of transgenic mice. RUNX1 is a powerful transcription factor implicated in diverse signaling pathways and cellular mechanisms that participate in lung development and pulmonary diseases. RUNX1 has recently been identified as a target regulator of fibrotic remodeling diseases, particularly in the kidney. However, the role of RUNX1 in pulmonary fibrosis is unclear. Pulmonary fibrosis is characterized by obscure nosogenesis, limited therapy, and poor prognosis. Moreover, the population of patients with pulmonary fibrosis is gradually increasing. Thus, there is an unmet need for therapeutic targets. In this review, we retrospectively discuss the alteration in RUNX1 mRNA expression in the RNA sequencing data of human fibrotic lungs and the protein levels in mouse pulmonary fibrosis. Subsequently, we focused on the interaction between RUNX1 and several signaling pathways involved in pulmonary fibrosis. Finally, this review highlights the therapeutic potential of RUNX1 as a target for slowing the progression of fibrotic lung disease.

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Keywords

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