The nuclear receptor 4A family members: mediators in human disease and autophagy
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Cellular & Molecular Biology Letters
Open Access
REVIEW LETTER
The nuclear receptor 4A family members: mediators in human disease and autophagy Liqun Chen1,2*† , Fengtian Fan1,2†, Lingjuan Wu1,2 and Yiyi Zhao1,2 *Correspondence: [email protected] † Liqun Chen and Fengtian Fan are co-first author. 1 College of Biological Science and Engineering, Fuzhou University, Fuzhou 350108, China Full list of author information is available at the end of the article
Abstract The Nuclear receptor 4A (NR4A) subfamily, which belongs to the nuclear receptor (NR) superfamily, has three members: NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor1). They are gene regulators with broad involvement in various signaling pathways and human disease responses, including autophagy. Here, we provide a concise overview of the current understanding of the role of the NR4A subfamily members in human diseases and review the research into their regulation of cell autophagy. A deeper understanding of these mechanisms has potential to improve drug development processes and disease therapy. Keywords: NR4A family, Autophagy, Human disease, Nur77, Nurr1, Nor1
Introduction Autophagy is an evolutionarily conserved catabolic process that attenuates cellular stress by digesting cytoplasmic contents and disposing of intracellular waste [1, 2]. The process involves lysosomal enzymes degrading pathogens, longevity proteins, damaged organelles and other components [3, 4]. Rapid adaptation to environmental changes to maintain homeostasis is key to the health and survival of cells and organisms. By maintaining a balance between synthesis and degradation, autophagy can regulate homeostasis [5]. The process of regulating autophagy is highly conserved, being found in all eukaryote cells [6, 7]. Most cells and tissues have basic autophagy activity under normal physiological conditions. A variety of stimuli can also induce autophagy: for example, cellular stress factors, including physiological stress (e.g., nutritional deficiencies, high temperature, high-density conditions and hypoxia), hormones (e.g., glucagon), and pharmacological agents (e.g., Torin 1 and rapamycin) [6]. Dysregulated autophagy is associated with infections, cancers, and neurodegenerative, metabolic, cardiovascular and lung diseases, among other conditions [3, 8]. The main steps of autophagy are: (1) induction of cell autophagy; (2) nucleation of autophagosomes; (3) amplification and completion of autophagosomes; (4) docking and fusion of autophagosomes and vacuoles; and (5) degradation and outflow of decomposition products [9].
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