Mechanisms of physiological and pathological cardiac hypertrophy

@article{Nakamura2018MechanismsOP,
  title={Mechanisms of physiological and pathological cardiac hypertrophy},
  author={Michinari Nakamura and Junichi Sadoshima},
  journal={Nature Reviews Cardiology},
  year={2018},
  volume={15},
  pages={387-407}
}
Cardiomyocytes exit the cell cycle and become terminally differentiated soon after birth. Therefore, in the adult heart, instead of an increase in cardiomyocyte number, individual cardiomyocytes increase in size, and the heart develops hypertrophy to reduce ventricular wall stress and maintain function and efficiency in response to an increased workload. There are two types of hypertrophy: physiological and pathological. Hypertrophy initially develops as an adaptive response to physiological… 

Cardiac Hypertrophy: from Pathophysiological Mechanisms to Heart Failure Development

TLDR
The underlying molecular mechanisms of pathological hypertrophy development and progression are summarized and can be applied in the development of future novel therapeutic strategies in both reversal and prevention.

A Case for Adaptive Cardiac Hypertrophic Remodeling Is CITED.

The postnatal heart responds to chronic hemodynamic stress by mounting a hypertrophic growth response. Two general types of cardiac hypertrophy have been described: physiological and pathological.1

Identification of circular RNAs in cardiac hypertrophy and cardiac fibrosis

TLDR
The crucial coexpression of circRNA–mRNA and its interaction with miRNA showed the possible mechanism of circRNAs in the process of cardiac dysfunction and may provide promising targets for the treatment of pathological cardiac hypertrophy and fibrosis.

Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

TLDR
Observations support the view that a low amount of oxyradical formation for a brief period may activate redox-sensitive mechanisms, which are associated with the development of cardiac hypertrophy.

The function of LncRNA-H19 in cardiac hypertrophy

TLDR
This review summarizes the current studies about the role of lncRNA-H19 in cardiac hypertrophy, including its pathophysiological processes and underlying pathological mechanism, including calcium regulation, fibrosis, apoptosis, angiogenesis, inflammation, and methylation.

Editorial: Cardiac Hypertrophy: From Compensation to Decompensation and Pharmacological Interventions

TLDR
Many studies have demonstrated that ventricular hypertrophy and remodeling is associated with a significantly increased risk of heart failure, malignant arrhythmia, and even sudden death, and is thought to be an independent risk factor for increasing morbidity and mortality of cardiovascular diseases.

Single-Cell Transcriptomics

TLDR
This study provides a framework for understanding how the transcriptional activity of individual cardiac cells is altered during pathological hypertrophy, and a reservoir of clinically relevant scRNA-seq data that can be used to generate and test novel hypotheses and potential clinical interventions for the management of patients with HF.

MicroRNAs in Cardiac Hypertrophy

TLDR
This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways.

GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway

TLDR
The role of GCN5 is elucidated in promotion of cardiac hypertrophy, thereby implying it to be a potential target for treatment.

Fibroblast growth factor 20 attenuates pathological cardiac hypertrophy by activating the SIRT1 signaling pathway

TLDR
Findings reveal a previously unknown protective effect of FGF20 on pathological cardiac hypertrophy by reducing oxidative stress through activation of the SIRT1 signaling pathway.
...

References

SHOWING 1-10 OF 371 REFERENCES

Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets

TLDR
New therapeutic approaches either entering clinical trials or in preclinical development, and the challenges that remain in translating these discoveries to new and approved therapies for heart failure are addressed.

Angiogenesis and Cardiac Hypertrophy: Maintenance of Cardiac Function and Causative Roles in Heart Failure

TLDR
Recent advances in understanding the regulatory mechanisms of coordinated myocardial growth and angiogenesis in the pathophysiology of cardiac hypertrophy and heart failure are summarized.

Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.

TLDR
It is submitted that suppression of load-induced ventricular hypertrophy warrants careful consideration as a therapeutic strategy, because several lines of evidence, preclinical and epidemiological, highlight the maladaptive features of chronic ventricularhypertrophy.

Physiological and pathological cardiac hypertrophy.

Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.

TLDR
Both heart size and cardiac function areAngiogenesis dependent, and disruption of coordinated tissue growth and angiogenesis in the heart contributes to the progression from adaptive cardiac hypertrophy to heart failure.

Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling.

TLDR
It is now clear that intercellular signaling and communication between these cell types are critical in the pathophysiology of ventricular hypertrophy and remodeling, and there is still much to be revealed about the specific roles of these celltypes and their overall contribution to the hypertrophic response.

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway.

TLDR
The role of the Akt signaling pathway is discussed, focusing on the regulation of cardiac growth, contractile function, and coronary angiogenesis, and how this signaling pathway contributes to the development of physiological/pathological hypertrophy and heart failure are discussed.

The adult heart responds to increased workload with physiologic hypertrophy, cardiac stem cell activation, and new myocyte formation

TLDR
Findings highlight the endogenous regenerative capacity of the adult heart, represented by the eCSCs, and the fact that the physiological cardiac adaptation to exercise stress is a combination of cardiomyocyte hypertrophy and hyperplasia (cardiomyocytes and capillaries).

Akt1 Is Required for Physiological Cardiac Growth

TLDR
These results establish Akt1 as a pivotal regulatory switch that promotes physiological cardiachypertrophy while antagonizing pathological hypertrophy.
...