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Related Experiment Video

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Microfluidic Model to Mimic Initial Event of Neovascularization

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Fluid Mechanical Forces and Endothelial Mitochondria: A Bioengineering Perspective.

Christopher G Scheitlin¹, Devi M Nair¹, Juan A Crestanello²

¹Laboratory of Vascular Mechanotransduction & Oxidative Stress, Department of Biomedical Engineering, The Ohio State University, Columbus, OH 43210 ; Davis Heart & Lung Research Institute, The Ohio State University, Columbus, OH 43210.

Cellular and Molecular Bioengineering

|December 23, 2014

Summary

Fluid shear stress impacts endothelial cells, affecting mitochondrial function and leading to cardiovascular diseases. Understanding these mechanisms can help develop new treatments for endothelial dysfunction.

Keywords:

Shear stress autophagy cardiovascular disease endothelial dysfunction ischemia/reperfusion mitochondrial fission mitophagy nitric oxide oxidative stress reactive oxygen species

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Area of Science:

Cardiovascular Science
Cell Biology
Mitochondrial Biology

Background:

Endothelial cell dysfunction underlies cardiovascular diseases like atherosclerosis and ischemia/reperfusion injury.
Fluid shear stress and altered hemodynamics are critical regulators of endothelial homeostasis.
Mitochondrial oxidative stress and altered mitochondrial network dynamics are linked to endothelial dysfunction.

Purpose of the Study:

To review the interplay between intracellular signaling pathways and mitochondrial dynamics in endothelial cells under shear stress.
To summarize evidence on how fluid shear stress regulates mitochondrial function and cell fate.
To explore the role of hemodynamics in endothelial mitochondrial physiology and redox state.

Main Methods:

Review of existing literature on endothelial cell biology, mitochondrial function, and cardiovascular disease.
Analysis of studies investigating the effects of fluid shear stress on endothelial cells.
Synthesis of data on intracellular Ca2+, nitric oxide, mitochondrial reactive oxygen species, mitochondrial fusion/fission, autophagy/mitophagy, and apoptosis.

Main Results:

Fluid shear stress significantly influences mitochondrial form and function in endothelial cells.
Interconnections exist among Ca2+, nitric oxide, mitochondrial reactive oxygen species, mitochondrial dynamics, and cell survival/apoptosis pathways.
Shear stress under physiological and pathological (reperfusion) conditions modulates these intracellular processes.

Conclusions:

Understanding the impact of hemodynamics on endothelial mitochondrial physiology is crucial for treating cardiovascular diseases.
Targeting shear stress-mediated pathways offers potential for novel therapeutic strategies against endothelial dysfunction.
This review highlights key molecular and cellular mechanisms linking hemodynamics to cardiovascular health.