Impact of the Angiotensin II Receptor Antagonist, Losartan, on Myocardial Fibrosis in Patients with End-Stage Renal Disease: Assessment by Ultrasonic Integrated Backscatter and Biochemical Markers

Shibasaki, Yasunobu; Nishiue, Takashi; Masaki, Hiroya; Tamura, Koji; Matsumoto, Noriko; Mori, Yoshihide; Nishikawa, Mitsushige; Matsubara, Hiroaki; Iwasaka, Toshiji

doi:10.1291/hypres.28.787

Cited by 57 publications

(45 citation statements)

References 43 publications

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“…2,24 Ang II is a central mediator of fibrosis in the heart, and blocking the actions of Ang II has shown efficacy in reducing cardiac fibrosis in various experimental models as well as in patients with myocardial disease. 25 Although many of the myocardial responses to increased stress are independent of Ang II, angiotensin receptor blockers represent the most efficient class of drugs to reduce the LV mass in patients with hypertension. 26 To understand the function of CTGF in more detail, we subjected mice to 4-week infusion of Ang II.…”

Section: Discussionmentioning

confidence: 99%

Connective Tissue Growth Factor Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in Pressure Overload–Induced Heart Failure

Szabò

Magga²,

Alakoski³

et al. 2014

Hypertension

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Connective tissue growth factor (CTGF) is involved in the pathogenesis of various fibrotic disorders. However, its role in the heart is not clear. To investigate the role of CTGF in regulating the development of cardiac fibrosis and heart failure, we subjected mice to thoracic aortic constriction (TAC) or angiotensin II infusion, and antagonized the function of CTGF with CTGF monoclonal antibody (mAb). After 8 weeks of TAC, mice treated with CTGF mAb had significantly better preserved left ventricular (LV) systolic function and reduced LV dilatation compared with mice treated with control immunoglobulin G. CTGF mAb–treated mice exhibited significantly smaller cardiomyocyte cross-sectional area and reduced expression of hypertrophic marker genes. CTGF mAb treatment reduced the TAC-induced production of collagen 1 but did not significantly attenuate TAC-induced accumulation of interstitial fibrosis. Analysis of genes regulating extracellular matrix proteolysis showed decreased expression of plasminogen activator inhibitor-1 and matrix metalloproteinase-2 in mice treated with CTGF mAb. In contrast to TAC, antagonizing the function of CTGF had no effect on LV dysfunction or LV hypertrophy in mice subjected to 4-week angiotensin II infusion. Further analysis showed that angiotensin II–induced expression of hypertrophic marker genes or collagens was not affected by treatment with CTGF mAb. In conclusion, CTGF mAb protects from adverse LV remodeling and LV dysfunction in hearts subjected to pressure overload by TAC. Antagonizing the function of CTGF may offer protection from cardiac end-organ damage in patients with hypertension.

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Section: Discussionmentioning

confidence: 99%

Connective Tissue Growth Factor Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in Pressure Overload–Induced Heart Failure

Szabò

Magga²,

Alakoski³

et al. 2014

Hypertension

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show abstract

“…Angiotensin receptor inhibitors such as losartan appear to be effective in reducing cardiac fibrosis in a variety of models in animals and in humans. 36,37 Thus, compared to generally antagonizing TGF␤ signaling, angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists may be useful approaches to control fibrotic disease. …”

Section: Angiotensin IImentioning

confidence: 99%

Potential Therapeutic Targets for Cardiac Fibrosis

Leask

2010

Circulation Research

602

309

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“…AQ is an automated online technique that analyzes the ultrasound backscatter to identify the blood-tissue interface of cardiac chambers and generate volume waveforms within a defined region of interest (12,13). The automated border detection system is activated and optimized by adjusting the total and lateral gain and temporal gain compensation.…”

Section: Acoustic Quantificationmentioning

confidence: 99%

Enhanced Left Atrial Reservoir, Increased Conduit, and Weakened Booster Pump Function in Hypertensive Patients with Paroxysmal Atrial Fibrillation

et al. 2008

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Impact of the Angiotensin II Receptor Antagonist, Losartan, on Myocardial Fibrosis in Patients with End-Stage Renal Disease: Assessment by Ultrasonic Integrated Backscatter and Biochemical Markers

Abstract: Myocardial fibrosis commonly occurs in patients with end-stage renal disease (ESRD) and has proven to

Cited by 57 publications

References 43 publications

Connective Tissue Growth Factor Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in Pressure Overload–Induced Heart Failure

Connective Tissue Growth Factor Inhibition Attenuates Left Ventricular Remodeling and Dysfunction in Pressure Overload–Induced Heart Failure

Potential Therapeutic Targets for Cardiac Fibrosis

Enhanced Left Atrial Reservoir, Increased Conduit, and Weakened Booster Pump Function in Hypertensive Patients with Paroxysmal Atrial Fibrillation

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