Journal
MOLECULES
Volume 22, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/molecules22010030
Keywords
SLE; cell death; apoptosis; necrosis; autophagy; epigenetics
Funding
- National Natural Science Foundation of China [81522038, 81430074, 81220108017, 81602767]
- National Basic Research Program of China [2014CB541904]
- Ph.D. Programs Foundation of Ministry of Education of China [20120162130003]
- Programs of Science-Technology Commission of Hunan province [2013FJ4202]
- National Key Clinical Specialty Construction Project of National Health and Family Planning Commission of the People's Republic of China
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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease involving multiple organs and tissues, which is characterized by the presence of excessive anti-nuclear autoantibodies. The pathogenesis of SLE has been intensively studied but remains far from clear. Increasing evidence has shown that the genetic susceptibilities and environmental factors-induced abnormalities in immune cells, dysregulation of apoptosis, and defects in the clearance of apoptotic materials contribute to the development of SLE. As the main source of auto-antigens, aberrant cell death may play a critical role in the pathogenesis of SLE. In this review, we summarize up-to-date research progress on different levels of cell deathincluding increasing rate of apoptosis, necrosis, autophagy and defects in clearance of dying cellsand discuss the possible underlying mechanisms, especially epigenetic modifications, which may provide new insight in the potential development of therapeutic strategies for SLE.
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