| REVIEW ARTICLE |
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| Year : 2018 | Volume
: 30
| Issue : 2 | Page : 61-65 |
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Activating transcription factor 3, an early cellular adaptive responder in ischemia/reperfusion-induced injury
Heng Lin1, Ching-Feng Cheng2
1 Department of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
2 Department of Pediatrics, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation; School of Medicine, Tzu Chi University, Hualien, Taiwan
Correspondence Address:
Dr. Ching-Feng Cheng
Department of Pediatrics, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, 707, Section 3, Chung-Yang Road, Hualien
Taiwan
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/tcmj.tcmj_37_18
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Recent studies have reported that ischemia/reperfusion (I/R) may act in the immune system where an exaggerated inflammatory response is initiated. With the activation of the immune system, damage-associated molecular patterns migrate and adhere to the I/R region, consequently inducing multiorgan injury. Emerging data indicate that upon I/R, stress-inducible proteins, including activating transcription factor 3 (ATF3), play essential roles in signaling during antiapoptotic, antimigration, and anti-inflammatory processes. Accumulating data suggest that ATF3 may be a potential target in I/R- or inflammation-induced organ dysfunction. This minireview focuses on the emerging evidence of the roles of ATF3 in multiple organs including the kidney, myocardium, and brain following I/R injury. In addition, this review addresses the role of ATF3 in chronic inflammation-induced pathophysiologies such as diabetes and atherosclerosis.
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