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Prolonged stress has long been shown to have major effects on the
development of both type of diabetes mellitus, Type 1 and Type 2.
Type 1 diabetes is an autoimmune disease that is characterized by
the immune system attacking self-antigens. There is a failure or
breakdown in immunological tolerance to allow this to happen.
Prolonged physical or emotional stress can activate the
hypothalamus-pituitary-adrenal (HPA) axis to induce production of
the stress hormone glucocorticoid, causing abrupt thymus involution
and result in escape of autoreactive T- cells. Though regulatory
T-cells (Treg) are present in the circulation, they are unable to
suppress the autoreative T-cells from initiating the destruction of
-cells and the subsequent development of Type 1 diabetes. Stress
also causes metabolic disturbances, including altered hepatic
glucose metabolism, increased peripheral insulin resistance and
hyperglycemia. Glucocorticoid is the potential contributor to the
chronic hyperglycemia that results in insulin resistance and -cell
dysfunction via the generation of oxidative stress which ultimately
leads to the development of Type 2 diabetes."
G Protein Coupled Receptors (GPCRs) are a large family of seven
transmembrane (TM) helical structural motif containing proteins
that regulate cellular communication. Based on sequence similarity
within the seven TM segment in human, the major five GPCR families
are rhodopsin, secretin, glutamate, adhesion and frizzled/taste.
GPCRs are principle signal transducer that activate senses of
sight, smell and test, and responsible for many signaling disorders
and diseases. Molecular mechanisms of GPCR activation are always
implicated as a therapeutic purpose to discover new drug targets.
Several molecular mechanisms and models of GPCR activation have
been proposed. Dimerization, protonation, conformations due to
intramolecular interaction and specific conformational changes are
thought to be responsible for receptor activation. In this review,
these mechanisms and proposed model systems are discussed in
detail.
Programmed cell death, which is termed as apoptosis, is essential
for normal development and maintenance of tissue homeostasis in
multicellular organisms. Aberrant regulation of this pathway is
linked to multiple human diseases, including cancer, autoimmunity,
neurodegenerative disorders and diabetes. Apoptosis is pursued by
two pathways; extrinsic and intrinsic pathway. The intrinsic
pathway of apoptosis mainly relies on mitochondria where Bcl-2
family proteins serve as the master regulators. Mitochondria mainly
execute their function through mitochondrial outer membrane
permeabilization (MOMP). MOMP leads to the release of several
apoptogenic factors from mitochondrial intermembrane space, such as
cytochrome c and Smac/Diablo, into the cytosol that activate
downstream caspase and promote cell death. Bcl-2 family proteins
play key role by regulating MOMP. The complex interaction among
pro-and anti-apoptotic Bcl-2 family members determine the
possibility of MOMP and thereby determine the cellular commitment
to apoptosis. This review focuses on the mitochondrial pathway of
apoptosis, mechanism of MOMP and its regulation by Bcl-2 family
proteins.
Psychological stress has extreme adverse consequences on health.
However, the molecular mechanisms that mediate and accelerate the
process of aging due to stress hormone are not well defined. This
review has focused on diverse molecular paths that come out in
response to chronic psychological stress via releasing of excessive
glucocorticoids (GCs), involved in the aging process. GCs suppress
transcription of nuclear cell adhesion molecules which impair
synaptic plasticity, memory formation, and cognitive ability.
Again, GCs promote muscle atrophy by means of motivating ubiquitin
proteasome system and can repress muscle protein synthesis by
inhibition of PI3-kinase/Akt pathway. GCs also inhibit
interleukin-2 synthesis through suppressing T cell receptor signal
that leads to loss of T cell activation, proliferation, and B-cell
activation. Moreover, GCs increase the expression of collagenase-3,
RANK ligand, and colony stimulating factor-1 that induce bone
resorption. In general, stress-induced GCs can play causal role for
aging and age-related disorders.
Chronic Psychological stress has several adverse effects both on
HIV- people and on HIV+ patient. When the HIV- people are
concerned, stress makes them more susceptible to HIV infection.
T-cells have CXCR4 receptor and Macrophage have CCR5 receptor which
can bind with both glucocorticoid and catecholamine hormone. HIV
has GP120 protein which has to bind with both CD4 and CXCR4/CCR5
receptor for its entry into the host cells. Mental stress increases
glucocorticoid and catecholamine concentration in blood. When these
stress hormones, glucocorticoid and catecholamine, bind with the
CXCR4/CCR5 receptors, cAMP signaling pathway gets activated. This
signal transduction pathway leads to the synthesis of more CXCR4
and CCR5 receptors by those cells, which in turn become more
susceptible to HIV infection. Stress inhibits Th2 when the cell
produces INF- as a response to viral attacks. So that other cells
remain vulnerable to viral infection. When T-cell count is
decreased in the blood, the body cannot protect itself from other
opportunistic infectious pathogens. As a result progression of AIDS
is increased."
Cancer is a class of diseases in which a group of cells display the
traits of uncontrolled growth, invasion, and sometimes metastasis.
These three malignant properties of cancers differentiate them from
benign tumors, which are self-limited, do not invade or
metastasize. Most cancers form a tumor but not all cancer e.g.
leukemia.Cancer may affect people at all ages, even fetuses, but
risk for the more common varieties tends to increase with age.
Nearly all cancers are caused by abnormalities in the genetic
material of the transformed cells. These abnormalities may be due
to the effects of carcinogens, such as tobacco smoke, radiation,
chemicals, or infectious agents. Other cancer-promoting genetic
abnormalities may be randomly acquired through errors in DNA
replication or are inherited and thus present in all cells from
birth. Complex interactions between carcinogens and the host genome
can explain mechanism of cancers develop after exposure to a known
carcinogen.This book addresses the biomolecular mechanisms of new
aspects of genetics in the initiation of Cancer and progression of
Tumor.
Atherosclerosis is a disease that causes medium-size and larger
blood vessels in the body to harden and narrow which is not a
clinical symptoms but it is the ultimate stage of any types of
coronary heart disease like stroke, heart attack, myocardial
infarction, paralysis and so on. In recent decades, there has been
increasing interest in exploring the relationship between
psychological stress and various health conditions. Extensive
studies support that behavioral and psychological factors
contribute significantly to the development and progression of
atherosclerosis. Psychological factors, specifically depression,
anxiety, personality factors, social isolation, and chronic and
sub-acute life stress, are known to be related to the risk of heart
disease. This spurred on the relentless effort to explore how
behaviour and biological systems could interact in the endeavour to
uncover more mysteries of the human body. This review addresses the
biomolecular mechanism of understanding the role of chronic
psychological stressors on the immune system and development of
atherosclerosis as well as established the relationship between the
chronic psychological stress and the atherosclerosis.
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