Transforming growth factor beta signaling in adult cardiovascular diseases and repair.

Doetschman T, Barnett JV, Runyan RB, Camenisch TD, Heimark RL, Granzier HL, Conway SJ, Azhar M
Cell Tissue Res. 2012 347 (1): 203-23

PMID: 21953136 · PMCID: PMC3328790 · DOI:10.1007/s00441-011-1241-3

The majority of children with congenital heart disease now live into adulthood due to the remarkable surgical and medical advances that have taken place over the past half century. Because of this, adults now represent the largest age group with adult cardiovascular diseases. It includes patients with heart diseases that were not detected or not treated during childhood, those whose defects were surgically corrected but now need revision due to maladaptive responses to the procedure, those with exercise problems and those with age-related degenerative diseases. Because adult cardiovascular diseases in this population are relatively new, they are not well understood. It is therefore necessary to understand the molecular and physiological pathways involved if we are to improve treatments. Since there is a developmental basis to adult cardiovascular disease, transforming growth factor beta (TGFβ) signaling pathways that are essential for proper cardiovascular development may also play critical roles in the homeostatic, repair and stress response processes involved in adult cardiovascular diseases. Consequently, we have chosen to summarize the current information on a subset of TGFβ ligand and receptor genes and related effector genes that, when dysregulated, are known to lead to cardiovascular diseases and adult cardiovascular deficiencies and/or pathologies. A better understanding of the TGFβ signaling network in cardiovascular disease and repair will impact genetic and physiologic investigations of cardiovascular diseases in elderly patients and lead to an improvement in clinical interventions.

MeSH Terms (15)

Aging Angiotensin II Animals Cardiac Rehabilitation Cardiovascular Diseases Epithelial-Mesenchymal Transition Gene Expression Genetic Variation Humans Mitogen-Activated Protein Kinases Mutation Receptors, Transforming Growth Factor beta Signal Transduction Smad Proteins Transforming Growth Factor beta

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