Not just the powerhouse of the cell: emerging roles for mitochondria in the heart.

@article{Hausenloy2010NotJT,
  title={Not just the powerhouse of the cell: emerging roles for mitochondria in the heart.},
  author={Derek J. Hausenloy and Marisol Ruiz-Meana},
  journal={Cardiovascular research},
  year={2010},
  volume={88 1},
  pages={
          5-6
        }
}
This editorial refers to the following articles in this issue which are part of the Review Focus on Mitochondria in Cardiac Disease: Emerging Concepts and Novel Therapeutic Targets: T. Miura et al .3, pp. 7–15; D. Hausenloy et al .4, pp. 67–74; S.-B. Ong and D. Hausenloy6, pp. 16–29; M. Ruiz-Meana et al .7, pp. 30–39; S.L. Hanninen et al .8, pp. 75–82; M.G. Rosca and C.L. Hoppel10, pp. 40–50; C.-H. Chen et al .13, pp. 51–57; S.M. Davidson14, pp. 58–66. It also refers to the following articles… 
View on PubMed
academic.oup.com
17 Citations
Background Citations
3

17 Citations

Citation Type

Citation Type

The Emerging Role of Mitochondrial Dynamics in Cardiovascular Disease
Mitochondrial Dysfunction and Inflammaging in Heart Failure: Novel Roles of CYP-Derived Epoxylipids
TLDR
Insight is provided into the potential roles N-3 and N-6 PUFA have modulating mitochondria, inflammaging and heart failure and emerging evidence suggests a protective role for CYP450 epoxygenase metabolites of N-1, 2, and 3 fatty acids, epoxylipids, which modulate various aspects of the immune system and protect mitochondria.
Mitochondrial dynamics and cell death in heart failure
TLDR
Growing evidence suggests that fusion/fission factors in adult cardiomyocytes play essential noncanonical roles in cardiac development, Ca2+ signaling, mitochondrial quality control and cell death, and pharmacological targeting of components of this intricate network may be a novel therapeutic modality for HF treatment.
Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart
TLDR
Increasing evidence suggests that these proteins by promoting mild uncoupling could reduce mitochondrial ROS generation and cardiomyocyte apoptosis and ameliorate thereby myocardial function.
Introduction to Mitochondria in the Heart
TLDR
In this introductory chapter to Mitochondria Role in Cardiovascular Diseases, primary defects in mitochondrial and nuclear genomes that cause alterations in major aspects of mitochondrial metabolism are discussed.
Activation of mitochondrial energy metabolism protects against cardiac failure
TLDR
Increased mitochondrial metabolism elicits an adaptive response due to mildly increased oxidative stress as a consequence of increased oxidative energy conversion, previously named mitohormesis, which activates protective mechanisms which counteract cardiotoxic stress and promote survival in states of experimental cardiomyopathy.
Effects of nuclear respiratory factor-1 on apoptosis and mitochondrial dysfunction induced by cobalt chloride in H9C2 cells
TLDR
It is demonstrated that NRF‑1 protected against CoCl2‑induced apoptosis, potentially by strengthening mitochondrial function to resist CoCl 2‑induced damage to H9C2 cells, and provides a possible way for the investigation of myocardial diseases.
Age-Dependent Protein Expression of Serine/Threonine Phosphatases and Their Inhibitors in the Human Cardiac Atrium
TLDR
There was a significant decline in PP2Ac and I2PP2A expression in older patients, whereas all other parameters remained unchanged with age, and it remains to be elucidated whether the decrease in the protein expression of I2pp2A might elevate cardiac PP2A activity in a detrimental way or is overcome by a reduced protein expression and thus a reduced activity of PP2 Ac.
Altered cardiac mitochondrial dynamics and biogenesis in rat after short-term cocaine administration
TLDR
Before any structural changes are observable in the myocardium, cocaine alters mitochondrial dynamics, elevates mitochondrial biogenesis, and induces the activation of UPRmt, which might reflect cardiac mitochondrial compensation to protect against the cardiotoxicity of cocaine.
Metformin and Glaucoma—Review of Anti-Fibrotic Processes and Bioenergetics
TLDR
Metformin, known for its use in type 2 diabetes, has come to the forefront of medical research in multiple organ systems and its application to glaucoma therapy is discussed, highlighting its effect on fibrotic signalling pathways, mitochondrial bioenergetics and NAD oxidation.
...
1
2
...

References

SHOWING 1-10 OF 20 REFERENCES
The SR-mitochondria interaction: a new player in cardiac pathophysiology.
TLDR
A more complete characterization of the structural arrangements responsible for SR-mitochondria interplay will allow better understanding of cardiac (patho)physiology but also should serve as a basis for the development of new treatments for cardiac diseases.
Mitochondrial cyclophilin-D as a critical mediator of ischaemic preconditioning
TLDR
The cyclophilin-D component of the mPTP is required by IPC to generate mitochondrial ROS and phosphorylate Akt and Erk1/2, major steps in the IPC signalling pathway.
Endothelial mitochondria and heart disease.
TLDR
Much remains to be done in understanding the contribution that mitochondria make to endothelial function, and new pharmaceutical approaches designed to target protective molecules such as ROS scavengers to the mitochondria promise to be effective in preventing heart disease.
Mitochondrial SIRT3 and heart disease.
TLDR
The known effects of SIRT3 in different tissues are reviewed and relate them to the protection of cardiomyocytes under stress and the only analogue whose increased expression has been associated with extended lifespan of humans is reviewed.
Mitochondrial morphology and cardiovascular disease.
TLDR
The current developments in this exciting new field of mitochondrial biology, the implications for cardiovascular physiology, and the potential for discovering novel therapeutic strategies for treating cardiovascular disease are reviewed.
Mitochondria in heart failure.
TLDR
Evaluated changes in mitochondrial morphology and alterations in the main components of mitochondrial energetics, such as substrate utilization and oxidative phosphorylation coupled with the level of respirasomes are evaluated in the context of their contribution to the chronic energy deficit and mechanical dysfunction in HF.
Mitochondrial reprogramming through cardiac oxygen sensors in ischaemic heart disease.
TLDR
The mechanisms underlying ischaemic preconditioning are examined, focusing, in particular, on those that involve the HIF pathway, such as adenosine signalling, sub-lethal ROS generation, and nitric oxide production.
Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis.
TLDR
Recent findings supporting roles of mitochondrial protein kinases in protection from myocardial necrosis after ischaemia/reperfusion are summarized and discussed.
Cardiac mitochondria and arrhythmias.
TLDR
Therapeutic strategies that prevent arrhythmias by preserving mitochondrial membrane potential in the face of oxidative stress are discussed, supporting the notion that treatments aimed at cardiac mitochondria have significant potential in attenuating electrical dysfunction in the heart.
What can we learn about cardioprotection from the cardiac mitochondrial proteome?
TLDR
The cardiac mitochondrial proteome is focused on with emphasis on changes associated with cell death and protection, and how proteomic data have contributed to addressing the role of mitochondria in cardioprotection is summarized.
...
1
2
...