TY - JOUR
T1 - Transcriptomic and proteomic analysis in the cardiovascular setting
T2 - Unravelling the disease?
AU - Marziliano, Nicola
AU - Grasso, Maurizia
AU - Pilotto, Andrea
AU - Porcu, Emanuele
AU - Tagliani, Marilena
AU - Disabella, Eliana
AU - Diegoli, Marta
AU - Pasotti, Michele
AU - Favalli, Valentina
AU - Serio, Alessandra
AU - Gambarin, Fabiana
AU - Tavazzi, Luigi
AU - Klersy, Catherine
AU - Arbustini, Eloisa
PY - 2009/5
Y1 - 2009/5
N2 - Whole gene expression analysis through microarray technologies revolutionized the manner of identifying changes in biological events and complex diseases, such as cardiovascular settings. These new methodologies may scan up to 35 000 transcripts at once rather than screening a small amount of genes one at a time. The ability of microarrays to provide a broad insight into the disease process directly within the tissues provides a unique insight into the intracellular perturbations of the cell organization and function and sheds an entirely unique new perspective on the heart failure process. Commonalities and differences at the molecular level will identify critical pathways of pathogenesis, and response to therapy, or both: indeed, gene expression profiling holds tremendous promise for classifying clinical phenotypes, developing prognostic predictors and, most importantly, providing novel unbiased insights into the mechanisms underlying heart disease and, eventually, novel causative genes. On the contrary, established proteomic technologies, together with the new alternative strategies currently under evaluation (i.e. metabolomics), are now making possible the translation of data obtained on the bench to the daily clinical routine with the discovery of new diagnostic/prognostic biomarkers (such as troponin for ACS and BNP for congestive heart failure) and the identification of new therapeutic approaches for combating heart diseases. Finally, genomic studies (including transcriptomics) together with proteomics should not represent a challenge for who is going to win the final battle, but rather they should provide a setting in which together and in a complementary fashion the final fight against heart disease can be won.
AB - Whole gene expression analysis through microarray technologies revolutionized the manner of identifying changes in biological events and complex diseases, such as cardiovascular settings. These new methodologies may scan up to 35 000 transcripts at once rather than screening a small amount of genes one at a time. The ability of microarrays to provide a broad insight into the disease process directly within the tissues provides a unique insight into the intracellular perturbations of the cell organization and function and sheds an entirely unique new perspective on the heart failure process. Commonalities and differences at the molecular level will identify critical pathways of pathogenesis, and response to therapy, or both: indeed, gene expression profiling holds tremendous promise for classifying clinical phenotypes, developing prognostic predictors and, most importantly, providing novel unbiased insights into the mechanisms underlying heart disease and, eventually, novel causative genes. On the contrary, established proteomic technologies, together with the new alternative strategies currently under evaluation (i.e. metabolomics), are now making possible the translation of data obtained on the bench to the daily clinical routine with the discovery of new diagnostic/prognostic biomarkers (such as troponin for ACS and BNP for congestive heart failure) and the identification of new therapeutic approaches for combating heart diseases. Finally, genomic studies (including transcriptomics) together with proteomics should not represent a challenge for who is going to win the final battle, but rather they should provide a setting in which together and in a complementary fashion the final fight against heart disease can be won.
KW - Cardiovascular disease
KW - Genomics
KW - Heart failure
KW - Microarrays
KW - Proteomics
KW - Transcriptomics
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UR - http://www.scopus.com/inward/citedby.url?scp=66349127121&partnerID=8YFLogxK
U2 - 10.2459/JCM.0b013e328324e972
DO - 10.2459/JCM.0b013e328324e972
M3 - Article
C2 - 19449458
AN - SCOPUS:66349127121
VL - 10
SP - 433
EP - 442
JO - Journal of Cardiovascular Medicine
JF - Journal of Cardiovascular Medicine
SN - 1558-2027
IS - 5
ER -