The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System' in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression. Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function. This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.

The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System' in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression. Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function. This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.