Growth regulators called angiotensin-converting enzyme 2 (ACE2, heart disease patients) are signaling cells that have greatly accelerated blood flow to the heart.
Yet, scientists still are not completely sure what enhancers ACE2 actually produces in blood vessels. It is well known that ACE2 increase blood flow in prions diseases as well as in one of the main types of brain cancer (neuronal tube cancer).
For years, scientists have known that ACE2 is heavily involved in blood vessel development, helping to switch back the cycle from growth to healing. It is now that researchers are giving them an edge by understanding a specific difference between clonal cell development in normal vascular growth and in HIV infection in a mouse model.
“The cell is in an advantageous position to absorb nutrients (platelets) and population growth-wide blood vessel formation from pathological cells (neurons of the heart) as well as normal brain’s cerebral blood vessels” says first author Marco Cardoni of the Italian Institute of Cancer (ICC) in Milan, Italy. “These characteristics might increase the rates of developing atrial fibrillation and the glomerular circulation.”
The findings are being presented at the Scientific Meeting on Neuro-Vascular Biology in Naples, organized by Prof. Clement Heilbronn of the Angewandte Chemie Aufgelheits zuwischen I-Wissenschaft (AACI), a German-Italian group supported by the Helmholtz Zentrum München.
The results are irreconcilable to the progression of this complex and don’t contradict current research. However, it is an important step towards creating new methods for treating patients at this stage of disease. “It would be a significant gain for patients if we could identify patients who are susceptible to developing the disease more easily as well as to identify patients who are already cured,” explains Marco Cardoni.
Antioxidant scavenging capacity of cell signals.
ACE2 is found in neuron cells and plays a role in accomplishing neuron growth, confirming earlier studies by the research group led by Dr. Antonio Giordano and Prof. Lorenz Schaller of the Albert Medical School (AMS).
“ACE2 augments the recognition of aspellic acid by the cell signals,” explains Prof. Cardoni. “ACE2 surface receptors are upstream mediators, which impact cell signaling and thus might also influence the reaction of leukocytes, neutrophiles, blood-vesicles and other patients.”
ACE2 plays a counterbalance role in leukocytes. Thus, the latter can replace leukocyte-mediated damage in cells, activating a pathological Th2 mechanism and helping to maintain vascular flow in the heart. “In vivo acute inflammation (e.g. with myocardial transfusion) or long-term chronic inflammation in patients with heart failure can result in a reduction of Th2 responses,” explains Marco Cardoni.
“ACE2 has a very specific membrane receptor (abnormal behavior of lipid receptors) attached to them and is a very attractive therapeutic target for the treatment of cardiac diseases,” explains Marco Cardoni. “Since heart-specific expression of ACE2 involves the receptor, we wondered how patients with reduced ACE2 overall have lower incidence of HLZ expansion. Also, the development of Th2 inflammatory conditions may be jeopardized by the drug.
Targeting the messenger receptor has different implications.
“Our results could be immediately relevant for treating patients with chronic atrial fibrillation as well as heart failure: We have identified the receptor and we have found a therapeutic target,” says Marco Cardoni. “Although it takes many years to develop compounds readily available to patients, we expect our key findings will be applicable to study the development of drugs for human and animal products with the goal of improving patients’ outcomes.”