No abstract available.
Autophagy* ; Neuralgia*

Autophagy is an active research area in the biomedical field as its role has been identified in many physiological and pathological processes. Accordingly, there is a growing demand to identify, quantify and manipulate the process accurately. Meanwhile, there is great interest in identifying compounds that modulate autophagy because they may have applications in the treatment of a variety of autophagy-related diseases. In this review, we summarize the current status of autophagy screening systems to facilitate identification of autophagy modulators.
Autophagy ; Humans

Autophagy is a highly conserved cellular self-digestion pathway, by which intracellular damaged proteins or organelles are delivered to lysosomes for degradation, so as to protect from various dangerous stimuli and maintain cellular homeostasis. Inflammation is a defensive response to injury or pathogens, through which various inflammatory mediators coordinate host defense and repair. However, uncontrolled inflammatory responses can lead to secondary damage and pathogenesis of inflammatory disease. Recent studies indicate that autophagy pathway and related proteins may play important roles in regulating immune response and controlling excessive inflammation. This review introduced research progress in the role of autophagy in regulating excessive inflammation and possible mechanisms.
Autophagy ; Homeostasis ; Humans ; Inflammation

Autophagy ; Liver Cirrhosis ; physiopathology

Autophagy ; Humans ; Liver Diseases ; MicroRNAs

OBJECTIVE: To study the role of autophagy in the development of systemic juvenile idiopathic arthritis (sJIA) by analyzing the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), myeloid differentiation factor 88 (MyD88), and suppressor of T-cell receptor signaling 1 (STS-1) in peripheral blood lymphocytes of children with sJIA. METHODS: A total of 26 children with sJIA were enrolled as the sJIA group, and 26 healthy children were enrolled as the control group. Western blot was used to measure the protein expression of LC3-II, STS-1, and MyD88 in peripheral blood lymphocytes. Immunofluorescence assay was used to measure the expression of LC3-II in the cytoplasm of lymphocytes. Pearson correlation analysis was used to assess the correlation between indices. RESULTS: Compared with the control group, the sJIA group had significant increases in the expression of LC3-II, STS-1, and MyD88 (P<0.05). In the sJIA group, the expression of LC3-II was positively correlated with that of MyD88 (r=0.478, P<0.05), and the expression of STS-1 was also positively correlated with that of MyD88 (r=0.817, P<0.05). CONCLUSIONS There is high expression of LC3-II in peripheral blood lymphocytes of children with sJIA, suggesting that the development of sJIA may be associated with excessive expression of autophagy. STS-1 may induce autophagy by activating some signaling pathways, and MyD88 may participate in autophagy through the Toll-like receptor signaling pathway.
Arthritis, Juvenile ; Autophagy ; Child ; Humans

Autophagy ; Child ; Humans ; Kidney Diseases

The role of autophagy is known to be highly complex and context-dependent, and may be characterized as both tumor suppression and tumor promotion in some tumors, such as breast cancer and prostate cancer. This review outlines recent advances in the studies of the involvement of autophagy in the development, progression and treatment of prostate cancer, focusing on autophagy modulation during androgen deprivation, with a special discussion on the regulatory effect of androgens on the autophagy of prostate cancer cells. A critical evaluation and analysis of the studies suggests that autophagy inhibition combined with androgen deprivation therapy is a promising approach to the treatment of prostate cancer.
Autophagy ; Humans ; Male ; Prostatic Neoplasms

Autophagy ; Humans ; Myocardial Reperfusion Injury

Autophagy ; Cardiovascular Diseases ; Humans ; MicroRNAs