Mitochondrial Metabolic Inhibition and Cardioprotection

@article{Lee2017MitochondrialMI,
  title={Mitochondrial Metabolic Inhibition and Cardioprotection},
  author={Sung Ryul Lee and Jin Han},
  journal={Korean Circulation Journal},
  year={2017},
  volume={47},
  pages={168 - 170}
}
Reperfusion is needed to initiate reflow of blood in cardiac arrest triggered by surgical intervention or pathologically-induced cardiac ischemia. However, subsequent reperfusion may lead not only to the recovery of ischemic cardiac tissue, but also to the paradoxical phenomenon of myocardial ischemia/reperfusion (IR) injury, including protracted organ recovery, myocardial stunning, and acute myocardial infarction (MI). Mortality due to acute MI remains substantial, and the prevalence of MI… 
3 Citations

Figures and Tables from this paper

Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis

The antifibrosis role of H2S is briefly addressed in order to gain insight into the development of novel strategies for the treatment of myocardial fibrosis.

Gaseous Signaling Molecules in Cardiovascular Function: From Mechanisms to Clinical Translation.

In this review, the basic aspects of CO, H2S, and NO, including their production and effects on enzymes, mitochondrial respiration and biogenesis, and ion channels are briefly addressed to provide insight into their biology with respect to the CVS.

Reviews of Physiology, Biochemistry and Pharmacology Vol. 174

This study analyzes the ezrin-meditated regulation of critical receptor complexes, including the epidermal growth factor receptor (EGFR), CD44, vascular cell adhesion molecule (VCAM), and the deleted in colorectal cancer (DCC) receptor to provide new insights for the design of novel therapeutic strategies for asthma treatment.

References

SHOWING 1-8 OF 8 REFERENCES

Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion.

This review addresses the emerging concept that modulation of mitochondrial respiration during and immediately following an episode of ischemia can attenuate the extent of myocardial injury by blocking electron transport and uncoupling respiration.

Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury

KCN pre-treatment reduced the severity of IR injury and was associated with enhanced expression and activity of mitochondrial antioxidase, suggesting the role of CcO in regulating IR injury through oxidative stress.

Time to Give Up on Cardioprotection? A Critical Appraisal of Clinical Studies on Ischemic Pre-, Post-, and Remote Conditioning.

The difficulties in translation of cardioprotection from animal experiments and proof-of-concept trials to clinical practice are discussed and it is suggested that it would be premature to give up on cardioprotsection.

Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery

An overview of the major topics discussed at this special meeting of leading pioneers in the field of cardioprotection to review and discuss the history of IPC, its evolution to IPost and RIC, myocardial reperfusion injury as a therapeutic target, and future targets and strategies for cardioprotsection is provided.

Cardiovascular effects of gasotransmitter donors.

This review is focused on the cardiovascular effects of NO, CO, and H(2)S and their donors as drug targeting the cardiovascular system.