Cardiovascular and Metabolic Disease Center
Mitochondrial Research Affinity Collaboration-Laboratories & Engineering

Home > 0

Mitochondrial dysfunction and redox signaling in atrial tachyarrhythmia

  • 작성자한진
  • 작성일2008-06-08 13:16:45
  • 조회수4007
  • 첨부파일첨부파일
http://www.news-medical.net/?id=37738 Researchers at the University Hospital of Magdeburg (Germany) have discovered that atrial tachycardia is associated with mitochondrial dysfunction and oxidative stress followed by the activation of the NF-kB signalling pathway with induction of NF-kB target gene expression in atrial tissue. Their study will appear in the May 08 issue of Experimental Biology and Medicine. Multiple tachycardia-associated factors appear to contribute to this response, which all are directly or indirectly linked to oxidative stress. Accordingly, blockade of the angiotensin II type 1 receptor, inhibition of L-type calcium channels, inhibition of NADPH oxidase, applications of antioxidants, and inhibition of NF-?? activation were all found to abolish or decrease the tachycardia-dependent changes in the atrial tissue. The interdisciplinary research team, led by Uwe Lendeckel, a professor of Experimental Internal Medicine and Andreas Goette, Deputy Chief of Cardiology, designed the study to determine the influence of tachyarrhythmia on endocardial dysfunction (called endocardial remodelling) and to decipher the molecular mechanism(s) that translate pathologically increased heart rates into myocardial/endocardial dysfunction. Endocardial dysfunction appears as a well recognised risk factor for thromboembolic events in patients with atrial fibrillation (AF). Therefore, the underlying pathophysiology of endocardial remodelling is of clinical importance. "The facts that equal results were observed in ex vivo atrial tissue from patients with AF and in ex vivo rapidly paced tissue samples from patients with sinus rhythm (SR), together with the observation that verapamil most potently prevented oxidative stress and associated signalling pathway activation, led us to conclude that the elevated frequency per se and concomitant Ca2+-overload precede and induce mitochondrial dysfunction and oxidative stress in AF" said Lendeckel. Goette added "Our results have several clinical implications. Atrial ischemia produces an increase in cellular calcium load and oxidative stress in the atria. Thereby, atrial ischemia provides a specific substrate for AF. Recent experimental and clinical data showed that calcium channel blockers have a specific efficacy to prevent AF in this specific situation. Thus, our data provide more information about the potential pathophysiologic mechanism explaining why calcium channel blockers are effective and useful to attenuate atrial cellular remodelling especially under conditions of increased cellular calcium load and oxidative stress". The authors say " the use of ex vivo human atrial tissue from patients with and without AF as well as the rapid pacing of atrial tissue slices to mimic AF ex vivo is a valuable approach to identify molecular and cellular effects that are solely due to the AF excluding the effects of concomitant cardiac diseases." Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine said "Professor Lendeckel, Professor Goette and colleagues have demonstrated that inward calcium current via L-type calcium channels contributes to oxidative stress and increased expression of oxidative stress markers and adhesion molecules during cardiac tachyarrhythmia.". He further stated "These observations are important to the understanding of the molecular mechanisms by which calcium overload and resulting mitochondrial dysfunction and resulting oxidative stress impact atrial remodelling during atrial fibrillation." Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. http://www.sebm.org
Total405 [ page17/27 ]
No. 제목 작성자 작성일 조회수
165 언제까지 공부해야하나? (1)첨부파일 2006.06.04 한진 2006.06.04 1,903
164 Mitochondrial physiology in tumourigenesis 2006.05.31 한진 2006.05.31 2,645
163 mitochondrial respiration 2006.05.31 한진 2006.05.31 7,414
162 커피 하루 1-3잔, 심혈관질환 예방에 도움 (1) 2006.05.27 김태호 2006.05.27 1,858
161 Cell - table of contents 2006.05.20 김형규 2006.05.20 7,164
160 science table of contents 2006.05.20 김형규 2006.05.20 4,983
159 Nature- table of contents 2006.05.20 김형규 2006.05.20 10,569
158 1번 염색체 해독 완료…인간게놈 ‘유전자 지도’ 완성 (2) 2006.05.18 김태호 2006.05.18 2,232
157 Scientists report Parkinson's discovery 첨부파일 2006.05.07 한진 2006.05.07 3,199
156 설창원 (2) 2006.05.04 한진 2006.05.04 1,879
155 Parkin’, ‘PINK1’ 단백질에 대한 논문이 동시에 나왔습니다. 참고바랍니다. (2)첨부파일 2006.05.04 한진 2006.05.04 4,401
154 Science of Sport: If you "feel the burn," you need to bulk up your mitochondria 첨부파일 2006.05.03 한진 2006.05.03 3,563
153 Possible target for future therapies aimed at delaying or stopping Alzheimer's disease 2006.05.02 한진 2006.05.02 1,895
152 Understanding Cell Death May Bring New Life To Kidney Treatment 2006.04.21 한진 2006.04.21 2,191
151 Agent Protects Parkinson's Neurons From Rotenone Toxicity 2006.04.21 한진 2006.04.21 3,352
처음 이전 11 12 13 14 15 16 17 18 19 20 다음 마지막