Chapter 17 Autophagy in Load-Induced Heart Disease

Research output: Contribution to journalArticle

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Abstract

The heart is a highly plastic organ capable of remodeling in response to changes in physiological or pathological demand. When workload increases, the heart compensates through hypertrophic growth of individual cardiomyocytes to increase cardiac output. However, sustained stress, such as occurs with hypertension or following myocardial infarction, triggers changes in sarcomeric protein composition and energy metabolism, loss of cardiomyocytes, ventricular dilation, reduced pump function, and ultimately heart failure. It has been known for some time that autophagy is active in cardiomyocytes, occurring at increased levels in disease. Yet the potential contribution of cardiomyocyte autophagy to ventricular remodeling and disease pathogenesis has only recently been explored. This latter fact stems largely from the recent emergence of tools to probe molecular mechanisms governing cardiac plasticity and to define the role of autophagic flux in the context of heart disease. In this chapter, we briefly review prominent mouse models useful in the study of load-induced heart disease and standard techniques used to assess whether a molecular or cellular event is adaptive or maladaptive. We then outline methods available for monitoring autophagic activity in the heart, providing detailed protocols for several techniques unique to working with heart and other striated muscles.

Original languageEnglish (US)
Pages (from-to)343-363
Number of pages21
JournalMethods in Enzymology
Volume453
Issue numberC
DOIs
StatePublished - 2009

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Autophagy
Cardiac Myocytes
Heart Diseases
Molecular Probes
Ventricular Remodeling
Striated Muscle
Workload
Cardiac Output
Energy Metabolism
Plastics
Dilatation
Heart Failure
Myocardial Infarction
Hypertension
Growth
Plasticity
Muscle
Pumps
Proteins
Fluxes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

Chapter 17 Autophagy in Load-Induced Heart Disease. / Zhu, Hongxin; Rothermel, Beverly A; Hill, Joseph A.

In: Methods in Enzymology, Vol. 453, No. C, 2009, p. 343-363.

Research output: Contribution to journalArticle

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