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HER2 is a member of the human epidermal growth factor receptor (HER/EGFR/ERBB) family. But contrary to other members of the ERBB family, HER2 does not directly bind ligand. HER2 activation results from heterodimerization with another ERBB member or by homodimerization when HER2 concentration are high, for instance in cancer. [8]
A slow heart rate of 60 or less beats per minute is defined as bradycardia. A fast heart rate of more than 100 beats per minute is defined as tachycardia. An arrhythmia is defined as one that is not physiological such as the lowered heart rate that a trained athlete may naturally have developed; the resting heart rates may be less than 60 bpm.
The human ERBB3 gene is located on the long arm of chromosome 12 (12q13). It is encoded by 23,651 base pairs and translates into 1342 amino acids. [5]During human development, ERBB3 is expressed in skin, bone, muscle, nervous system, heart, lungs, and intestinal epithelium. [6]
Trastuzumab downregulates neuregulin-1 (NRG-1), which is essential for the activation of cell survival pathways in cardiomyocytes and the maintenance of cardiac function. NRG-1 activates the MAPK pathway and the PI3K/AKT pathway as well as focal adhesion kinases (FAK). These are all significant for the function and structure of cardiomyocytes.
Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.
It employs pacemaker cells that produce electrical impulses, known as cardiac action potentials, which control the rate of contraction of the cardiac muscle, that is, the heart rate. In most humans, these cells are concentrated in the sinoatrial (SA) node, the primary pacemaker, which regulates the heart’s sinus rhythm.
Parasympathetic activation. If the heart is experiencing anoxia, hypercapnia (increased CO 2) or acidosis, the heart cells will enter a state of dysfunction and not work properly. Correct sarcomere crossbridges will not form the heart becomes less efficient (leading to myocardial failure). Loss of parts of the myocardium.
Several agents called "heart rate reducing agents" act by specifically inhibiting f-channel function. [3] Ivabradine is the most specific and selective I f inhibitor and the only member of this family that is now marketed for pharmacological treatment of chronic stable angina in patients with normal sinus rhythm who have a contraindication or ...