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See detailThe molecular basis of myocardial hypertrophy and heart failure.
Ritter, Oliver; Neyses, Ludwig UL

in Trends in molecular medicine (2003), 9(7), 313-21

Heart failure (HF) is the inability of the heart to cope with the metabolic demands of the periphery. It is the common end-stage of many frequent cardiac diseases and is characterized by relentless ... [more ▼]

Heart failure (HF) is the inability of the heart to cope with the metabolic demands of the periphery. It is the common end-stage of many frequent cardiac diseases and is characterized by relentless progression. Mechanisms of progression include renal sodium and water retention, neurohumoral activation and alterations of the protein composition (gene programme) of the heart itself. In this review, we explain the often confusing terminology in the subject, briefly touch upon the peripheral mechanisms of HF, and then focus on the changes in the gene programme of the failing heart and the molecular mechanisms leading to them. Understanding the basic processes underlying HF will help uninitiated readers to gain insight into recent novel approaches to its treatment. [less ▲]

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See detailParkinson's disease: one biochemical pathway to fit all genes?
Krüger, Rejko UL; Eberhardt, Olaf; Riess, Olaf et al

in Trends in molecular medicine (2002), 8(5), 236-40

Although originally discounted, hereditary factors have emerged as the focus of research in Parkinson's disease (PD). Genetic studies have identified mutations in alpha-synuclein and ubiquitin C-terminal ... [more ▼]

Although originally discounted, hereditary factors have emerged as the focus of research in Parkinson's disease (PD). Genetic studies have identified mutations in alpha-synuclein and ubiquitin C-terminal hydrolase as rare causes of autosomal dominant PD and mutations in parkin as a cause of autosomal recessive PD. Functional characterization of the identified disease genes implicates the ubiquitin-mediated protein degradation pathway in these hereditary forms of PD and also in the more common sporadic forms of PD. Subsequent identification of further loci in familial PD and diverse genetic factors modulating the risk for sporadic PD point to substantial genetic heterogeneity in the disease. Thus, new candidate genes are expected to encode proteins either involved in ubiquitin-mediated protein degradation or sequestrated in intracytoplasmic protein aggregations. Future identification of disease genes is required to confirm this hypothesis, thereby unifying the clinical and genetic heterogeneity of PD, including the common sporadic form of the disease, by one biochemical pathway. [less ▲]

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