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Introduction to e-Series A: Cardiovascular Diseases, Volume Four Part 2: Regenerative Medicine

Posted in Acute Myocardial Infarction, Biological Networks, Gene Regulation and Evolution, Ca2+ triggered activation, Calcium Signaling, Calmodulin Kinase and Contraction, Cardiac & Vascular Repair Tools Subsegment, Cardiac muscle regeneration, Cardiomyopathy, Cardiovascular Pharmacogenomics, Cardiovascular Research, Cell Biology, Signaling & Cell Circuits, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Circulating Progenitor Cells, Coagulation Therapy and Internal Bleeding, Competition in regenerative stem cell science, Computational Biology/Systems and Bioinformatics, Curation, De novo synthesis, Diabetes Mellitus, Discovery process, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Delivery Platform Technology, Endothelial cells, Epigenetics and Cardiovascular Risks, Experimental validation, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Testing: Methodology for Diagnosis, HTN, Medical Devices R&D and Inventions, Molecular Genetics & Pharmaceutical, Na-K transport, Na-K-ATPase, Nitric Oxide in Health and Disease, Nutrition, Origins of Cardiovascular Disease, PCI, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmacotherapy of Cardiovascular Disease, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Proteomics, Regenerative Biology and Medicine, Resident-cell-based, Stem Cells for Regenerative Medicine, tagged Absorb™ Bioresorbable Vascular Scaffold, Acute coronary syndrome, Acute decompensated heart failure, Angioplasty, Array-comparative genomic hybridization, Ca2+/calmodulin-dependent protein kinase, Cardiac & Vascular Repair, cardiac arrhythmias, cardiac biomarkers, cardiac myocyte regeneration, cardiomyocyte transformation, cardiovascular complications, Cardiovascular Risk Reduction, cEPC as Biomarker, Circulating Progenitor Endothelial Cells, comparative genomic hybridization, complement activation, endothelial cell, Endothelial Cell Coagulation Activation, functional genomics, Genome Biology, Genome engineering, Human Umbilical Vein Endothelial Cells (HUVECS), Induced pluripotent stem cells (iPS), regenerative medicine, Therapeutic Potential of cEPCs on April 27, 2014| Leave a Comment »

Introduction to e-Series A: Cardiovascular Diseases, Volume Four Part 2: Regenerative Medicine

Author and Curator: Larry H Bernstein, MD, FCAP

and

Curator: Aviva Lev-Ari, PhD, RN

This document is entirely devoted to medical and surgical therapies that have made huge strides in

simplification of interventional procedures,
reduced complexity, resulting in procedures previously requiring surgery are now done, circumstances permitting, by medical intervention.

This revolution in cardiovascular interventional therapy is regenerative medicine. It is regenerative because it is largely driven by

the introduction into the impaired vasculature of an induced pleuripotent cell, called a stem cell, although
the level of differentiation may not be a most primitive cell line.

There is also a very closely aligned development in cell biology that extends beyond and including vascular regeneration that is called synthetic biology. These developments have occurred at an accelerated rate in the last 15 years. The methods of interventional cardiology were already well developed in the mid 1980s. This was at the peak of cardiothoracic bypass surgery.

Research on the endothelial cell,

endothelial cell proliferation,
shear flow in small arteries, especially at branch points, and
endothelial-platelet interactions

led to insights about plaque formation and vessel thrombosis.

Much was learned in biomechanics about the shear flow stresses on the luminal surface of the vasculature, and there was also

the concomitant discovery of nitric oxide,
oxidative stress, and
the isoenzymes of nitric oxide synthase (eNOS, iNOS, and nNOS).

It became a fundamental tenet of vascular biology that

atherogenesis is a maladjustment to oxidative stress not only through genetic, but also
non-genetic nutritional factors that could be related to the balance of omega (ω)-3 and omega (ω)-6 fatty acids,
a pro-inflammatory state that elicits inflammatory cytokines, such as, interleukin-6 (IL6) and c-reactive protein(CRP),
insulin resistance with excess carbohydrate associated with type 2 diabetes and beta (β) cell stress,
excess trans- and saturated fats, and perhaps
the now plausible colonic microbial population of the gastrointestinal tract (GIT).

There is also an association of abdominal adiposity,

including the visceral peritoneum, with both T2DM and with arteriosclerotic vessel disease,
which is presenting at a young age, and has ties to
the effects of an adipokine, adiponectin.

Much important work has already been discussed in the domain of cardiac catheterization and research done to

prevent atheroembolization.and beyond that,
research done to implant an endothelial growth matrix.

Even then, dramatic work had already been done on

the platelet structure and metabolism, and
this has transformed our knowledge of platelet biology.

The coagulation process has been discussed in detailed in a previous document. The result was the development of a

new class of platelet aggregation inhibitors designed to block the activation of protein on the platelet surface that
is critical in the coagulation cascade.

In addition, the term long used to describe atherosclerosis, atheroma notwithstanding, is “hardening of the arteries”. This is particularly notable with respect to mid-size arteries and arterioles that feed the heart and kidneys. Whether it is preceded by or develops concurrently with chronic renal insufficiency and lowered glomerular filtration rate is perhaps arguable. However, there is now a body of evidence that points to

a change in the vascular muscularis and vessel stiffness, in addition to the endothelial features already mentioned.

This has provided a basis for

targeted pharmaceutical intervention, and
reduction in salt intake.

So we have a group of metabolic disorders, which may alone or in combination,

lead to and be associated with the long term effects of cardiovascular disease, including
congestive heart failure.

This has been classically broken down into forward and backward failure,

depending on decrease outflow through the aorta (ejection fraction), or
decreased venous return through the vena cava,

which involves increased pulmonary vascular resistance and decreased return into the left atrium.

This also has ties to several causes, which may be cardiac or vascular. This document, as the previous, has four pats. They are broadly:

Stem Cells in Cardiovascular Diseases
Regenerative Cell and Molecular Biology
Therapeutics Levels In Molecular Cardiology
Research Proposals for Endogenous Augmentation of circulating Endothelial Progenitor Cells (cEPCs)

As in the previous section, we start with the biology of the stem cell and the degeneration in cardiovascular diseases, then proceed to regeneration, then therapeutics, and finally – proposals for augmenting therapy with circulating endogenous endothelial progenitor cells (cEPCs).

stem cells

regeneration

Therapeutics

augmentation

Key pathways involving NO

stem cellLlin28

1479-5876-10-175-1-l translational research with feedback loops

Tranlational Research -Lab to Bedside

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Macrovascular Disease – Therapeutic Potential of cEPCs: Reduction Methods for CV Risk

Posted in Bio Instrumentation in Experimental Life Sciences Research, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Frontiers in Cardiology and Cardiovascular Disorders, Health Economics and Outcomes Research, HTN, Medical and Population Genetics, Nitric Oxide in Health and Disease, Origins of Cardiovascular Disease, Pharmaceutical Industry Competitive Intelligence, Pharmacotherapy of Cardiovascular Disease, Population Health Management, Genetics & Pharmaceutical, Resident-cell-based, tagged Aviva Lev-Ari, Cardiovascular Risk Reduction, Doctor of Philosophy, Endothelial progenitor cell, Macrovascular Disease, Mol Cell Cardiol, Stem cell treatments, Therapeutic Potential of cEPCs on July 2, 2012| 29 Comments »

Macrovascular Disease – Therapeutic Potential of cEPCs: Reduction Methods for CV Risk

Curator: Aviva Lev-Ari, PhD, RN

An Investigation of the Potential of circulating Endothelial Progenitor Cells (cEPCs) as a Therapeutic Target for Pharmacological Therapy Design for Cardiovascular Risk Reduction: A New Multimarker Biomarker Discovery

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