Neurohormones, Cytokines and Programmed Cell Death in Heart Failure: A New Paradigm for the Remodeling Heart

  title={Neurohormones, Cytokines and Programmed Cell Death in Heart Failure: A New Paradigm for the Remodeling Heart},
  author={Marco Valgimigli and Salvatore Curello and Claudio Ceconi and Laura Agnoletti and Laura Comini and Tiziana Bachetti and Elisa Merli and Roberto Ferrari},
  journal={Cardiovascular Drugs and Therapy},
Marco Valgimigli1, Salvatore Curello2, Claudio Ceconi2, Laura Agnoletti3, Laura Comini3, Tiziana Bachetti3, Elisa Merli1, and Roberto Ferrari1,3 1Chair of Cardiology, University of Ferrara, Cardiology and Intensive Cardiology Care Unit, S. Anna Hospital, Italy; 2Chair of Cardiology, University of Brescia, Spedali Civili Hospital, Italy; 3Cardiovascular Physiopatholgy Research Center, Salvatori Maugeri Foundation, Gussago (BS), Italy 
Pathophysiological role and clinical relevance of cytokines in hypertensive heart failure. A combined clinical and experimental study
It is hypothesized that proinflammatory cytokine activation is pathophysiologically important and clinically relevant in hypertensive heart failure, however, cytokineactivation may differ between the young and the elderly.
Immune activation and inflammatory system in chronic heart failure: novel pathophysiological hypotheses generate new therapeutic options
  • M. Piepoli
  • Medicine
    International journal of clinical practice
  • 2007
A complete review of the current knowledge of the immune activation and inflammatory system in CHF is presented with the potential and novel therapeutic approaches.
Apoptosis in Cardiac Disease: From Basics to Clinics—An Editorial Commentary
  • M. Paul
  • Medicine
    Cardiovascular Drugs and Therapy
  • 2004
The “mini-series” of articles on apoptosis in heart disease published in this issue of Cardiovascular Drugs and Therapy, which is based on lectures given in a special session at the last annual congress of the International Society of Card cardiovascular Pharmacotherapy held in Amsterdam provides a splendid tutorial and summary of the current state of the art.
Autonomic imbalance and immune activation in chronic heart failure - pathophysiological links.
These two phenomena predict prognosis and represent therapeutic targets in the syndrome of CHF, and it is hypothesised they are closely related.
Myocardial Fas and Cytokine Expression in End‐Stage Heart Failure: Impact of LVAD Support
While interleukin (IL)‐6 was significantly reduced by LVAD support, the impact of support on Fas was highly variable and tightly linked to tumor necrosis factor (TNF).
Role of inflammation and extracellular matrix remodelling in dogs with cardiac and systemic diseases
Evidence of myocardial inflammation and remodelling with regional quantitative differences in dogs with cardiac and systemic diseases is provided and a role for leptin is suggested in canine cardiac disease.
The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress in cardiovascular diseases
The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress especially in heart failure with preserved ejection fraction are discussed and the nature of the crosstalk of these signaling processes as well as possible therapeutic implications for cardiovascular medicine are emphasized.


Prospects for cardioreparation.
In spontaneously hypertensive rats with left ventricular hypertrophy and adverse structural remodeling of the cardiac interstitium, angiotensin-converting enzyme inhibition has resulted in restoration of myocardial integrity and stiffness toward normal.
Remodeling and reparation of the cardiovascular system.
It is proposed that these are therapeutic goals that may reduce cardiovascular morbidity and mortality and the primary goal of therapy should be to preserve or restore tissue structure and function.
Circulating tumour necrosis factor‐α (cachectin) in myocardial infarction
The results show that extensive myocardial infarction induces the release of the monocyte/macrophage‐derived polypeptide hormone TNF into circulation, and this finding may be clinically relevant with respect to systemic metabolic consequences of myocardia infarct.
Serum from patients with severe heart failure downregulates eNOS and is proapoptotic: role of tumor necrosis factor-alpha.
Serum from patients with severe CHF downregulates eNOS expression and increases apoptosis, and high levels of TNF-alpha likely play a role, but they cannot be the only factor responsible.
Loss of a gp130 Cardiac Muscle Cell Survival Pathway Is a Critical Event in the Onset of Heart Failure during Biomechanical Stress
Cardiac myocyte apoptosis is a critical point in the transition between compensatory cardiac hypertrophy and heart failure and gp130-dependent cytokines may represent a novel therapeutic strategy for preventing in vivo heart failure.
Increased circulating cytokines in patients with myocarditis and cardiomyopathy.
Granulocyte colony stimulating factor was often increased in myocarditis, cardiomyopathies, acute myocardial infarction, and angina pectoris--suggesting activation of macrophages and/or endothelial cells--but this increase was not specific to these diseases.
Tumour necrosis factor and inducible nitric oxide synthase in dilated cardiomyopathy
The localisation of iNOS and T NF-alpha within cardiac tissues in DCM suggests that TNF-alpha contributes to both the low contractility and the tendency to thromboembolism in these patients.
Cardiocyte adaptation to chronically altered load.
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    Annual review of physiology
  • 1987
The long-standing multidisciplinary interest in myocardial hypertrophy re­ cently has evolved from a description of specific forms of this entity to a more general consideration of the basic
Pathophysiological Correlates of Increased Serum Tumor Necrosis Factor in Patients With Congestive Heart Failure: Relation to Nitric Oxide‐Dependent Vasodilation in the Forearm Circulation
The significant correlation between serum concentrations of TNFα and forearm blood flow responses to acetylcholine and nitroglycerin suggests that both the inducible and the constitutive forms of nitric oxide synthase are involved in the regulation of peripheral vasomotor tone in patients with CHF.
Tumour necrosis factor alpha in severe congestive cardiac failure.
The stimulus resulting in enhanced plasma concentrations of TNF alpha in congestive heart failure remains unclear and concentrations at any particular time were not prognostic.