Fibrosis and heart failure

@article{Segura2012FibrosisAH,
  title={Fibrosis and heart failure},
  author={Ana Maria Segura and O. Howard Frazier and L. Maximilian Buja},
  journal={Heart Failure Reviews},
  year={2012},
  volume={19},
  pages={173-185}
}
The extracellular matrix (ECM) is a living network of proteins that maintains the structural integrity of the myocardium and allows the transmission of electrical and mechanical forces between the myocytes for systole and diastole. During ventricular remodeling, as a result of iterations in the hemodynamic workload, collagen, the main component of the ECM, increases and occupies the areas between the myocytes and the vessels. The resultant fibrosis (reparative fibrosis) is initially a… 
Mechanisms of Cardiac Fibrosis and Heart Failure
TLDR
The structure and function of the cardiac ECM from development to various pathological states is reviewed as well as new findings in the study of reverse cardiac remodelling following unloading of the left ventricle are highlighted.
Remodelling of the Cardiac Extracellular Matrix: Role of Collagen Degradation and Accumulation in Pathogenesis of Heart Failure
TLDR
An overview of the mechanisms involved in myocardial fibrosis, the disease-dependent nature and consequence of different types of Fibrosis, clinical biomarkers of collagen turnover, and potential therapeutic approaches in managing the myocardium are provided.
The fibrosis-cell death axis in heart failure
TLDR
The interaction between cardiac fibrosis, cardiomyocyte hypertrophy and cell death, and potential strategies for tackling progressive cardiac remodeling and HF are described.
Mechanisms of cardiac collagen deposition in experimental models and human disease.
The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart
TLDR
The current status of knowledge of mechanotransduction signaling pathways in cardiac fibroblasts that culminate in pro-fibrotic gene expression are reviewed.
Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity—Pathogenesis and Involvement of the Extracellular Matrix
TLDR
Excessive collagen deposition in the extracellular matrix (ECM) in the course of obesity may increase the stiffness of the myocardium and thereby deteriorate the heart diastolic function and facilitate the occurrence of HFpEF.
Inhibitor of lysyl oxidase improves cardiac function and the collagen/MMP profile in response to volume overload.
TLDR
In conclusion, this study demonstrated key cardioprotective effects of LOX inhibition against adverse cardiac remodeling due to chronic VO and improved ventricular collagen and matrix metalloproteinase/tissue inhibitor of metalliproteinase profiles.
Cardiomyocyte damage control in heart failure and the role of the sarcolemma
TLDR
A novel perspective on sar colemma remodelling is presented by considering whether targeting proteins that regulate sarcolemma injury-repair may hold promise for developing new strategies to attenuate HF progression.
...
...

References

SHOWING 1-10 OF 164 REFERENCES
Cellular and molecular pathways to myocardial necrosis and replacement fibrosis
TLDR
It is now further recognized that Ca2+ overloading of cardiac myocytes and mitochondria serves as a prooxidant and which is counterbalanced by an intrinsically coupled Zn2+ entry serving as antioxidant, and the prospect of raising antioxidant defenses by increasing intracellular Zn 2+ with adjuvant nutriceuticals can be preferentially exploited to uncouple this intrinsically coupled Ca2–Zn2- dyshomeostasis.
Cardiac interstitium in health and disease: the fibrillar collagen network.
  • K. Weber
  • Biology, Medicine
    Journal of the American College of Cardiology
  • 1989
A look between the cardiomyocytes: the extracellular matrix in heart failure.
TLDR
The extracellular matrix of the heart dynamically interacts with various cellular components of the myocardium, including the myocytes and connective tissue cells, to provide a focus to its often overlooked contribution to the development and progression of heart failure and thereby its potential role as a target for therapy for heart failure.
Regression of fibrosis and hypertrophy in failing myocardium following mechanical circulatory support.
  • B. Bruckner, S. Stetson, G. Torre-Amione
  • Medicine, Biology
    The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
  • 2001
Cardiac remodeling and failure From molecules to man (Part II).
Mechanisms of Disease: pathologic structural remodeling is more than adaptive hypertrophy in hypertensive heart disease
TLDR
The clinical relevance of ventricular fibrosis is that it might contribute to the increased cardiac risk of patients with hypertensive heart disease and the therapeutic strategies aimed to promote its reduction are discussed.
Targeting pathological remodeling: concepts of cardioprotection and reparation.
  • K. Weber
  • Biology, Medicine
    Circulation
  • 2000
TLDR
Together with thehypertrophy of left ventricular myocytes, these iterations in tissue structure in HHD create a pathological hypertrophy that predisposes to an enhanced risk of adverse cardiovascular events, including myocardial infarction, diastolic and/or systolic ventricular dysfunction, symptomatic heart failure, and arrhythmias.
Pathological Hypertrophy and Cardiac Interstitium: Fibrosis and Renin‐Angiotensin‐Aldosterone System
TLDR
It can be concluded that arterial hypertension together with elevated circulating aldosterone are associated with cardiac fibroblast involvement and the resultant heterogeneity in tissue structure and the stage is set to prevent pathological LVH resulting from myocardial fibrosis as well as to reverse it.
Extracellular matrix and cardiovascular diseases.
  • H. Ju, I. Dixon
  • Medicine, Biology
    The Canadian journal of cardiology
  • 1996
TLDR
The accumulation of ECM in the cardiovascular system plays an important role in the development of heart failure after myocardial infarction and hypertension, as well as in vascular hypertrophy and restenosis.
...
...