Cardiomyopathy with Prominent Autophagic Degeneration, Accompanied by an Elevated Plasma Brain Natriuretic Peptide Level Despite the Lack of Overt Heart Failure

Saijo, Mieko; Takemura, Genzou; Koda, Masahiko; Okada, Hideshi; Miyata, Shusaku; Ohno, Yasushi; Kawasaki, Masanori; Tsuchiya, Kunihiko; Nishigaki, Kazuhiko; Minatoguchi, Shinya; Goto, Kazuko; Fujiwara, Hisayoshi

doi:10.2169/internalmedicine.43.700

Cited by 32 publications

(19 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, in contrast to other studies, Beclin-1 has been shown to induce autophagic cell death in the heart. 101 This study, among others 97,102,103 highlights the point that autophagy is still not well understood in the heart, and as suggested by Matsui et al, 67 there may be two separate autophagic modes depending on the activity of AMPK under ischemia compared to reperfusion, which may directly relate to autophagy's protective or deleterious effect on the myocardium.…”

Section: The Role Of Cell Death In the Heartmentioning

confidence: 52%

Molecular regulation of autophagy and apoptosis during ischemic and non-ischemic cardiomyopathy

Shaw¹,

Kirshenbaum²

2008

Autophagy

View full text Add to dashboard Cite

A significant understanding of the genetic signaling pathways governing the extrinsic and intrinsic apoptotic pathways has been established. In recent years, the role of apoptosis in the heart during ischemic and non-ischemic cardiomyopathies has been under investigation and reported to contribute to ventricular remodeling and heart failure. Autophagy has been recently characterized as an essential cellular process in the heart, but whether autophagy functions as a pro-death or pro-survival program during disease conditions is still not completely understood. The mitochondrial death protein Bnip3 has been implicated in both apoptosis and autophagy, and its role in both processes is also discussed.

show abstract

Section: The Role Of Cell Death In the Heartmentioning

confidence: 52%

Molecular regulation of autophagy and apoptosis during ischemic and non-ischemic cardiomyopathy

Shaw¹,

Kirshenbaum²

2008

Autophagy

View full text Add to dashboard Cite

show abstract

“…Analysis of human samples has afforded additional evidence that autophagic cell death contributes to HF pathogenesis (30,67). In patients with isolated aortic valve stenosis and varying degrees of left ventricular systolic dysfunction, cell loss, mainly due to autophagy and oncosis, was associated with the progression of left ventricular systolic dysfunction (5).…”

Section: Autophagy In Cardiovascular Diseasementioning

confidence: 99%

Autophagy in cardiovascular biology

Lavandero

Chiong

Rothermel³

et al. 2015

J. Clin. Invest.

286

211

View full text Add to dashboard Cite

Autophagy in the vascular systemEndothelial cells. Autophagy can be regulated in vascular endothelial cells by compounds circulating in the bloodstream or localized within the subendothelial layer of atherosclerotic plaque. For example, in cultured HUVECs, vitamin D increases beclin 1, a key comCardiovascular disease is the leading cause of death worldwide. As such, there is great interest in identifying novel mechanisms that govern the cardiovascular response to disease-related stress. First described in failing hearts, autophagy within the cardiovascular system has been widely characterized in cardiomyocytes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, and macrophages. In all cases, a window of optimal autophagic activity appears to be critical to the maintenance of cardiovascular homeostasis and function; excessive or insufficient levels of autophagic flux can each contribute to heart disease pathogenesis. In this Review, we discuss the potential for targeting autophagy therapeutically and our vision for where this exciting biology may lead in the future.

show abstract

“…Autophagy is also important in cell death; autophagic cell death has been recognized as caspaseindependent or programed cell death type II [107]. Cardiomyocyte death showing characteristics of autophagy is reported in human heart failure due to dilated cardiomyopathy, valvular heart disease, hypertensive heart disease, and chronic ischemia [81,[108][109][110]. Autophagy is activated by a variety of extracellular and intracellular stimuli, including nutrient deprivation, insulin, and growth factors, via PI3K and mTOR signaling (Fig.…”

Section: Metabolic Features Of Programed Cell Survivalmentioning

confidence: 99%

Return to the fetal gene program protects the stressed heart: a strong hypothesis

et al. 2007

View full text Add to dashboard Cite

A common feature of the hemodynamically or metabolically stressed heart is the return to a pattern of fetal metabolism. A hallmark of fetal metabolism is the predominance of carbohydrates as substrates for energy provision in a relatively hypoxic environment. When the normal heart is exposed to an oxygen rich environment after birth, energy substrate metabolism is rapidly switched to oxidation of fatty acids. This switch goes along with the expression of "adult" isoforms of metabolic enzymes and other proteins. However, the heart retains the ability to return to the "fetal" gene program. Specifically, the fetal gene program is predominant in a variety of pathophysiologic conditions including hypoxia, ischemia, hypertrophy, and atrophy. A common feature of all of these conditions is extensive remodeling, a decrease in the rate of aerobic metabolism in the cardiomyocyte, and an increase in cardiac efficiency. The adaptation is associated with a whole program of cell survival under stress. The adaptive mechanisms are prominently developed in hibernating myocardium, but they are also a feature of the failing heart muscle. We propose that in failing heart muscle at a certain point the fetal gene program is no longer sufficient to support cardiac structure and function. The exact mechanisms underlying the transition from adaptation to cardiomyocyte dysfunction are still not completely understood.

show abstract

Cardiomyopathy with Prominent Autophagic Degeneration, Accompanied by an Elevated Plasma Brain Natriuretic Peptide Level Despite the Lack of Overt Heart Failure

Cited by 32 publications

References 16 publications

Molecular regulation of autophagy and apoptosis during ischemic and non-ischemic cardiomyopathy

Molecular regulation of autophagy and apoptosis during ischemic and non-ischemic cardiomyopathy

Autophagy in cardiovascular biology

Return to the fetal gene program protects the stressed heart: a strong hypothesis

Contact Info

Product

Resources

About