Aging and disease

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01 February 2011. VOL 2, ISSUE 2 Previous Issue Next Issue

Nitroproteins Identified in Human Ex-smoker Bronchoalveolar Lavage Fluid
Xianquan Zhan, Dominic M. Desiderio

2011, 2 (2): 100-115

PDF (932KB)
Myocardial Infarction in the Elderly
Amelia Carro, Juan Carlos Kaski

2011, 2 (2): 116-137

PDF (1130KB)
Ischemic Preconditioning in the Younger and Aged Heart
Pasquale Abete, Gianluca Testa, Francesco Cacciatore, David Della-Morte, Gianluigi Galizia, Assunta Langellotto, Franco Rengo

2011, 2 (2): 138-148

PDF (607KB)
Dietary Factors and the Risk of Coronary Heart Disease
Jinesh Kochar, J. Michael Gaziano, Luc Djoussé

2011, 2 (2): 149-157

PDF (384KB)
Aging and Cardiac Fibrosis
Anna Biernacka, Nikolaos G Frangogiannis

2011, 2 (2): 158-173

PDF (830KB)
The Mitoscriptome in Aging and Disease
Raghavan Raju, Bixi Jian, William Hubbard, Irshad Chaudry

2011, 2 (2): 174-180

PDF (470KB)
Aging and Transplantation – A Topic for Biomedicine or Bioethics?
William J. Hubbard, Nassrin Dashti

2011, 2 (2): 181-185

PDF (375KB)

Cover Illustration

01 February 2011. Vol.2 No.2
The aging heart is characterized by morphological and structural changes that lead to its functional decline and are associated with diminished ability to meet increased demand. Extensive evidence, derived from both clinical and experimental studies suggests that the aging heart undergoes fibrotic remodeling. Age-dependent accumulation of collagen in the heart leads to progressive increase in ventricular stiffness and impaired diastolic function. Increased mechanical load, due to reduced arterial compliance, and direct senescence-associated fibrogenic actions appear to be implicated in the pathogenesis of cardiac fibrosis in the elderly. Evolving evidence suggests that activation of several distinct molecular pathways may contribute to age-related fibrotic cardiac remodeling. Reactive oxygen species, chemokine-mediated recruitment of mononuclear cells and fibroblast progenitors, transforming growth factor (TGF)-β activation, endothelin-1 and angiotensin II signaling mediate interstitial and perivascular fibrosis in the senescent heart. Reduced collagen degradation may be more important than increased de novo synthesis in the pathogenesis of aging-associated fibrosis. In contrast to the baseline activation of fibrogenic pathways in the senescent heart, aging is associated with an impaired reparative response to cardiac injury and defective activation of reparative fibroblasts in response to growth factors. Because these reparative defects result in defective scar formation, senescent hearts are prone to adverse dilative remodeling following myocardial infarction. Understanding the pathogenesis of interstitial fibrosis in the aging heart and dissecting the mechanisms responsible for age-associated healing defects following cardiac injury are critical in order to design new strategies for prevention of adverse remodeling and heart failure in elderly patients.

[Detail]

Cover Illustration

The aging heart is characterized by morphological and structural changes that lead to its functional decline and are associated with diminished ability to meet increased demand. Extensive evidence, derived from both clinical and experimental studies suggests that the aging heart undergoes fibrotic remodeling. Age-dependent accumulation of collagen in the heart leads to progressive increase in ventricular stiffness and impaired diastolic function. Increased mechanical load, due to reduced arterial compliance, and direct senescence-associated fibrogenic actions appear to be implicated in the pathogenesis of cardiac fibrosis in the elderly. Evolving evidence suggests that activation of several distinct molecular pathways may contribute to age-related fibrotic cardiac remodeling. Reactive oxygen species, chemokine-mediated recruitment of mononuclear cells and fibroblast progenitors, transforming growth factor (TGF)-β activation, endothelin-1 and angiotensin II signaling mediate interstitial and perivascular fibrosis in the senescent heart. Reduced collagen degradation may be more important than increased de novo synthesis in the pathogenesis of aging-associated fibrosis. In contrast to the baseline activation of fibrogenic pathways in the senescent heart, aging is associated with an impaired reparative response to cardiac injury and defective activation of reparative fibroblasts in response to growth factors. Because these reparative defects result in defective scar formation, senescent hearts are prone to adverse dilative remodeling following myocardial infarction. Understanding the pathogenesis of interstitial fibrosis in the aging heart and dissecting the mechanisms responsible for age-associated healing defects following cardiac injury are critical in order to design new strategies for prevention of adverse remodeling and heart failure in elderly patients.