2011
DOI: 10.1111/j.1540-8167.2011.02187.x
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Differential Structural Remodeling of the Left‐Atrial Posterior Wall in Patients Affected by Mitral Regurgitation with or Without Persistent Atrial Fibrillation: A Morphological and Molecular Study

Abstract: The LAPW of MR patients with or without AF shows considerable SR. The former has more severe histopathological changes and higher levels of proteins involved in SR, thereby reaching a threshold beyond which the sinus impulse cannot normally activate atrial myocardium.

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Cited by 68 publications
(53 citation statements)
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“…Interstitial fibrosis, chronic inflammation, and cellular glycogen accumulation were noted in the dilated left atria, but myocyte hypertrophy, myolysis, and necrosis were absent. In contrast, myocyte hypertrophy, dedifferentiation, and degeneration and fibrosis are described in pigs with surgically created chronic MR 223 and patients with MR. 12,224 High-density oligonucleotide microarrays, enrichment analysis, and a differential proteomics approach were used to characterize the molecular regulatory mechanisms and biological processes involved in the atrial myopathy that is seen in pigs with moderate to severe chronic (6 and 12 months) MR. 225 Renin-angiotensin-system and peroxisome proliferatoractivated receptor signalling pathways and genes involved in the regulation of apoptosis, autophagy, oxidative stress, cell growth, and carbohydrate metabolism were differentially regulated. 225 MLC2V (a marker of cardiac hypertrophy and important in the regulation of myocyte contractility) had the highest fold change in the MR pigs.…”
Section: Atrial Cardiomyopathy Due To Valvular Heart Diseasementioning
confidence: 99%
“…Interstitial fibrosis, chronic inflammation, and cellular glycogen accumulation were noted in the dilated left atria, but myocyte hypertrophy, myolysis, and necrosis were absent. In contrast, myocyte hypertrophy, dedifferentiation, and degeneration and fibrosis are described in pigs with surgically created chronic MR 223 and patients with MR. 12,224 High-density oligonucleotide microarrays, enrichment analysis, and a differential proteomics approach were used to characterize the molecular regulatory mechanisms and biological processes involved in the atrial myopathy that is seen in pigs with moderate to severe chronic (6 and 12 months) MR. 225 Renin-angiotensin-system and peroxisome proliferatoractivated receptor signalling pathways and genes involved in the regulation of apoptosis, autophagy, oxidative stress, cell growth, and carbohydrate metabolism were differentially regulated. 225 MLC2V (a marker of cardiac hypertrophy and important in the regulation of myocyte contractility) had the highest fold change in the MR pigs.…”
Section: Atrial Cardiomyopathy Due To Valvular Heart Diseasementioning
confidence: 99%
“…Although microcirculation dysfunction in the atrium is still controversial in AF, 7 capillary rarefaction has been frequently found in the LA posterior wall of AF patients. 8 Additionally, chronic AF patients have a lower LA capillary density. 9 Accordingly, aging-related microcirculatory dysfunction may play a role in the pathophysiology of AF.…”
mentioning
confidence: 99%
“…Our interest is supported by experimental studies on animal models and humans, which have suggested a key role of MMPs in their onset and progression [7][8][9][10][11][12][13][14][15]. However, in literature, there are few data [16,17] showing associations of SNPs in MMP genes with MVD susceptibility.…”
Section: Discussionmentioning
confidence: 74%
“…Particularly, Levine and colleagues have recently underlined that MVDs are the result of a 'living valve', which with advancing age shows active changes mediated both by valvular endothelial and interstitial cells and alterations in composition and turnover of elements of extracellular matrix [6]. Accordingly, in surgically excised human myxomatous tissues, an overexpression of transforming growth factor-β cytokine (TGF-β) pathway, an increased release of metalloproteinases (MMPs), and down-expression of related inhibitors (TIMPs), responsible for degeneration of collagen and elastin structures, have been observed [7][8][9][10][11][12][13][14][15]. Increased systemic and tissue levels of MMPs in cases affected by degenerative sporadic MVDs and with stenosis or regurgitation complications have been also assessed [7][8][9][10][11][12][13][14][15].…”
Section: Introductionmentioning
confidence: 99%
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