PMID- 18322650
OWN - NLM
STAT- MEDLINE
DCOM- 20080709
LR  - 20220330
IS  - 1420-682X (Print)
IS  - 1420-682X (Linking)
VI  - 65
IP  - 10
DP  - 2008 May
TI  - Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation.
PG  - 1489-508
LID - 10.1007/s00018-008-7408-8 [doi]
AB  - Electrical, contractile and structural remodeling have been characterized in 
      atrial fibrillation (AF), and the latter is considered to be the major 
      contributor to AF persistence. Recent data show that interstitial fibrosis can 
      predispose to atrial conduction impairment and AF induction. The interplay 
      between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, 
      tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial 
      extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, 
      transforming growth factor-beta1, inflammation and oxidative stress are 
      particularly important for ECM dysregulation and atrial fibrotic remodeling in 
      AF. Therefore, we review recent advances in the understanding of the atrial 
      fibrotic process, the major downstream components in this remodeling process, and 
      the expression and regulation of MMPs and TIMPs. We also describe the activation 
      of bioactive molecules in both clinical studies and animal models to modulate 
      MMPs and TIMPs and their effects on atrial fibrosis in AF.
FAU - Lin, C-S
AU  - Lin CS
AD  - Department of Biological Science and Technology, National Chiao Tung University, 
      No. 75 Po-Ai Street, Hsinchu, Taiwan. lincs@mail.nctu.edu.tw
FAU - Pan, C-H
AU  - Pan CH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Switzerland
TA  - Cell Mol Life Sci
JT  - Cellular and molecular life sciences : CMLS
JID - 9705402
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (Tissue Inhibitor of Metalloproteinases)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (ras GTPase-Activating Proteins)
RN  - 11128-99-7 (Angiotensin II)
RN  - 9041-90-1 (Angiotensin I)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
RN  - IJ3FUK8MOF (angiotensin I (1-7))
SB  - IM
MH  - Angiotensin I/pharmacology
MH  - Angiotensin II/genetics/physiology
MH  - Animals
MH  - Antihypertensive Agents/pharmacology
MH  - Atrial Fibrillation/genetics/*physiopathology
MH  - Endomyocardial Fibrosis/genetics/*physiopathology
MH  - Heart Atria/*pathology
MH  - Humans
MH  - Inflammation/genetics/physiopathology
MH  - Matrix Metalloproteinases/genetics/physiology
MH  - Models, Biological
MH  - Oxidative Stress/genetics/physiology
MH  - Peptide Fragments/pharmacology
MH  - Signal Transduction/genetics
MH  - Tissue Inhibitor of Metalloproteinases/genetics/physiology
MH  - Transforming Growth Factor beta1/physiology
MH  - Ventricular Remodeling/*genetics
MH  - ras GTPase-Activating Proteins/genetics/physiology
RF  - 224
EDAT- 2008/03/07 09:00
MHDA- 2008/07/10 09:00
CRDT- 2008/03/07 09:00
PHST- 2008/03/07 09:00 [pubmed]
PHST- 2008/07/10 09:00 [medline]
PHST- 2008/03/07 09:00 [entrez]
AID - 10.1007/s00018-008-7408-8 [doi]
PST - ppublish
SO  - Cell Mol Life Sci. 2008 May;65(10):1489-508. doi: 10.1007/s00018-008-7408-8.