Abstract
Sirtuins are the class III of histone deacetylases whose deacetylate of histones is dependent on nicotinamide adenine dinucleotide (NAD+). Among seven sirtuins, SIRT1 plays a critical role in modulating a wide range of physiological processes, including apoptosis, DNA repair, inflammatory response, metabolism, cancer, and stress. Neuroinflammation is associated with many neurological diseases, including ischemic stroke, bacterial infections, traumatic brain injury, Alzheimer's disease (AD), and Parkinson's disease (PD). Recently, numerous studies indicate the protective effects of SIRT1 in neuroinflammation-related diseases. Here, we review the latest progress regarding the anti-inflammatory and neuroprotective effects of SIRT1. First, we introduce the structure, catalytic mechanism, and functions of SIRT1. Next, we discuss the molecular mechanisms of SIRT1 in the regulation of neuroinflammation. Finally, we analyze the mechanisms and effects of SIRT1 in several common neuroinflammation-associated diseases, such as cerebral ischemia, traumatic brain injury, spinal cord injury, AD, and PD. Taken together, this information implies that SIRT1 may serve as a promising therapeutic target for the treatment of neuroinflammation-associated disorders.
Highlights
Inflammation is a physiological response of the immune system to harmful infectious and noninfectious stimuli
We summarized the latest evidence of the beneficial roles of silent information regulator 1 (SIRT1) in the regulation of neuroinflammation and neurodegenerative diseases
We focused on the regulatory effect of SIRT1 in the inflammation response of central nervous system (CNS)
Summary
Inflammation is a physiological response of the immune system to harmful infectious and noninfectious stimuli. In response to such stimuli, macrophages, immune cells, and vascular cells take concerted reactions to maintain or restore the integrity of tissue [1]. There are several innate immune cells in the brain, including astrocytes, microglia, macrophages, natural killer (NK) cells, mast cells, and oligodendrocytes [10]. Acute neuroinflammation is a key response to clear pathogens and to repair tissue damage. Many studies have indicated that SIRT1 could regulate the inflammation response in multiple tissues and cells [16]. This study may serve as a useful foundation for the design of a drug for future neuroinflammation and neurodegenerative disease treatments
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