Coronary artery disease (CAD) is the most common cause of morbidity and mortality in industrialized societies. Collateral arteries function as "natural bypasses" effectively restoring the blood flow to compromised tissues and play an important physiologic role in promoting survival and protecting tissues from ischemic damage. Circulating monocytes have been suggested to play a role in the collateral formation. Abnormalities in monocyte function then may be one of the factors responsible for abnormal collateral growth in certain patient subsets.
Dartmouth researchers have now shown, via comprehensive characterizations of the molecular determinates of the human CAD monocyte transcriptome, that the monocyte transcriptome of closely matched patients with CAD that possess abundant collateral circulation is significantly different from the transcriptome of collateral-poor CAD subjects. The key differences included significant alterations in transcriptional regulation of specific determinates of monocyte biology that could be directly related to abnormalities in intracellular transport, apoptosis, and cell proliferation. These consistent molecular alterations can now be used to advance both the understanding of the basic biology of coronary collateral artery formation as well as the clinically relevant aspects of coronary collateralization in coronary artery disease. Moreover, the specific transcripts, proteins and profiles serve as markers for determining collateral artery formation in coronary artery disease.
This technology is claimed in the published PCT Application No. PCT/US2007/080506. We are seeking an industrial partner interested in its commercialization. (Ref: J380)
Last Updated: 7/24/12