인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2008.12
- 수록면
- 1,131 - 1,138 (8page)
이용수
초록· 키워드
Diabetic complications are a leading cause of blindness, renal failure, and nerve damage. Additionally, diabetesaccelerated atherosclerosis leads to increased risk of myocardial infarction, stroke, and limb amputation. At the present time, 4 main molecular mechanisms have been implicated in hyperglyceamia-mediated vascular damage. In particular, advanced glycation endproducts (AGE), which are formed by complex, heterogeneous, sugar-derived protein modifications, have been implicated as a major pathogenic process for diabetic complications. Recently, AGE inhibitors such as aminoguanidin, ALT-946, and pyridoxamine have been reported. Such an integrating paradigm provides a new conceptual framework for future research on diabetes complications and on discovering drugs to prevent the progression of AGE-induced maladies.
#advanced glycation endproduct
#diabetes mellitus
#diabetic complication
#inhibitor
#reactive oxygen species (ROS)
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목차
- Abstract
- Introduction
- Mechanisms of Diabetic Complications
- AGEs and Diabetic Complications
- Formation of Various AGEs in vivo and Related Toxicity
- AGE Formation During Diabetic Conditions
- ROS and Diabetes
- Pharmacological Inhibition of AGEs
- Conclusion
- Acknowledgments
- References
참고문헌
참고문헌 신청최근 본 자료
UCI(KEPA) : I410-ECN-0101-2013-573-000858236