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10 Genesis Growth And Future of Cardiodiabetic Medicine

Curriculum development of ACMDC –an Advanced of the TNF superfamily is the TNF-like weak inducer
certificated Course in the Prevention and Management of apoptosis (TWEAK/ TNFS12) and its receptor
of Diabetes and Cardiovascular Disease. Fn14. We have observed that Fn14 and TWEAK are
expressed in macrophages and smooth muscle cells
Diabetologists, cardiologists, lipidologists and renal in carotid atherosclerotic plaques, and could be novel
physicians joint specialist clinics run at hospital mediators of atherosclerosis. In addition, we have
centres, Primary Care Trust (PCT) one-stop clinics.
observed that soluble TWEAK (sTWEAK) is released
in lower amount by carotid plaques than normal
The Future of Cardiovascular Medicine endarteries. Subsequent measurement of sTWEAK in
plasma showed a reduced concentration in subjects
Novel Biomarkers Of Cardiovascular with carotid stenosis compared with healthy subjects.
Diseases Furthermore, in a test population of 106 asymptomatic
JESUS EGIDO, JOSE LUIS MARTIN-VENTURA, LUIS subjects, we showed that sTWEAK concentrations
MIGUEL BLANCO-COLIO Fundación Jiménez Diaz, negatively correlated with the carotid intima-media
Autonoma University, Madrid, Spain thickness, suggesting that sTWEAK could be a
potential biomarker of subclinical atherosclerosis.
Assessment of vascular risk in asymptomatic The identification of novel biomarkers along with
patients is a major challenge for prevention of traditional risk factors and imaging techniques, could
cardiovascular events. These events arise from the help to target vulnerable patients and monitor the
disruption of atherosclerotic plaques that contain beneficial effects of pharmacological agents.
Cardio-diabetology research reports and training
unit 25 numerous inflammatory cells. Inflammatory
and resident cells (endothelial and vascular smooth Genomics of Cardiovascular Disease &
muscle cells) release different proteins that can Diabetes Mellitus
generate a chronic inflammatory response in the The most studied and replicated locus associated
injured artery. with MI and CAD is locatedon chromosome 9p21.3 .
Measurement of circulating markers of inflammation This locus is near the CDKN2A and CDKN2B genes,
may provide some insights into this process. contains no annotated genes, and is not associated
Interaction between members of the tumor necrosis with established CVD risk factors such as plasma
factor (TNF) superfamily and their receptors lipoproteins, or hypertension. Interestingly, it has also
elicits diverse biologic actions that participate in been associated with diabetes.
atherosclerosis development. Fas and its ligand are Diabetes can be classified as type 1 diabetes (T1D),
typical members of the TNF superfamily. Proteins type 2 diabetes (T2D), latent autoimmune diabetes
secreted by cells implicated in atherosclerotic lesions, in adults (LADA), mature onset diabetes of the
including soluble Fas (sFas) and soluble Fas ligand young (MODY). For T1D, the major susceptibility
(sFasL), circulate in small, but detectable, amounts. locus is related to HLA class II genes at 6p21, which
We have observed that sFas concentrations are accounts for more than 30%-50% of the genetic risk
increased and sFasL are decreased in subjects at high of T1D. Also, more than 40 non-HLA susceptibility
cardiovascular risk, suggesting that these proteins gene markers have been associated with the trait .
may be novel markers of vascular injury. 15
In addition, patients with familial combined T2D involves complex genetics. There is an intricate
hyperlipidemia or carotid atherosclerosis have interaction between the environment and genetic
decreased circulating sFasL levels, probably background, understood as the contribution of many
indicating endothelial dysfunction. To confirm this different genes.
hypothesis, we have recently analyzed whether the Susceptibility loci: Genome-wide association studies
forearm vasodilatory response to reactive hyperemia (GWAS). successfully identified approximately 75
(an indicator of endothelial function), is associated susceptibility loci related to T2DM. Examples of
with soluble sFasL plasma concentrations in subjects candidate genes are KCNJ11 (potassium inwardly
with coronary artery disease. rectifying channel, subfamily J, member 11), TCF7L2
There was a linear trend for the increase of sFasL (transcription factor 7-like 2, the strongest T2D locus
and forearm reactive hyperemia which suggest that identified to date), IRS1 (insulin receptor substrate
sFasL plasma concentrations could be a potential 1), MTNR1B (melatonin-receptor gene), PPARG2
biomarker of endothelial function. Another member (peroxisome proliferator-activated receptor gamma
2), IGF2BP2 (insulin-like growth factor two binding

GCDC 2017