64
persons, the fat mass causes low glucose transport, stops insulin to perform its action,
and increases FFA and others [37]. The hyperglycemic condition develops when the
glucose level rises from its range and insulin sensitivity decreases [38]. In a diabetic
person, at cellular level mitochondrial respiration and its density decrease which also
decreases the energy production in the form of ATP and mRNA. Insulin resistance
and type 2 diabetic patients at the cellular level have reduced mitochondrial respiration, ATP production and mitochondrial density and mRNA [39]. Oxidative stress
always increases with the intake of the high- calorie diet which causes OXPHOS to
increase its enzyme protein expression. In the brain, the increase in reactive oxygen
species in the OXPHOS process is the major cause of oxidative damage of mtDNA
[40]. When the insulin signaling pathway is inhibited by an excess of reactive species and also interferes with acetyl CoA to being oxidized in obese and diabetic
persons results in increased lipid and diacylglycerol [1]. In diabetic and obese conditions, mitochondrial synthesis has impaired [35]. PGC-1α also involved in the generation of mitochondria [41]. In addition, mitochondrial dysfunction may be the
target of therapeutic measures to treat diseases such as obesity and diabetes.
Mitochondrial Involvement in Cardiovascular Complications
Heart diseases are also a major issue around the globe. There are many factors which
are involved in cardiovascular diseases, these are an environmental and genetic factor. From studies, it is confirmed that oxidative stress is directly proportional to an
increased number of mtDNA. The heart can generate many reactive species in the
heart cells including cardiac myocytes, endothelial cells, and neutrophils. There are
many in vivo and in vitro researches available that documented that oxidative stress
has a high impact on reducing reactive species in the cells [6]. The reactive species
in the heart are generated when ETC complexes I and III get disrupted [42]. In
accordance with this, other mechanisms are also involved in damaging heart tissues
by producing reactive oxygen species, these are NADPH oxidase, xanthine oxidoreductase, or NOS. The increased reactive oxygen species decreases the antioxidant
capacity of cell and causes cell injury which results in an alteration in gene expression, damaging mtDNA and abnormality in the functioning of endothelial cells [6],
this results in failing heart muscle called myocardium [43]. Additionally, reactive
oxygen species activate contractile functions, activate enzymes and transcription
factors. Thus, the reactive oxygen species could be involved in cardiovascular
diseases.
Mitochondrial Involvement in Stroke
Stroke is the main cause of death in developing countries. There are many factors
that induce a stroke. They may be economical, physiological, or others. Among
these, oxidative stress is also the contributing factor which causes a stroke by tissue
G. Murtaza et al.
persons, the fat mass causes low glucose transport, stops insulin to perform its action,
and increases FFA and others [37]. The hyperglycemic condition develops when the
glucose level rises from its range and insulin sensitivity decreases [38]. In a diabetic
person, at cellular level mitochondrial respiration and its density decrease which also
decreases the energy production in the form of ATP and mRNA. Insulin resistance
and type 2 diabetic patients at the cellular level have reduced mitochondrial respiration, ATP production and mitochondrial density and mRNA [39]. Oxidative stress
always increases with the intake of the high- calorie diet which causes OXPHOS to
increase its enzyme protein expression. In the brain, the increase in reactive oxygen
species in the OXPHOS process is the major cause of oxidative damage of mtDNA
[40]. When the insulin signaling pathway is inhibited by an excess of reactive species and also interferes with acetyl CoA to being oxidized in obese and diabetic
persons results in increased lipid and diacylglycerol [1]. In diabetic and obese conditions, mitochondrial synthesis has impaired [35]. PGC-1α also involved in the generation of mitochondria [41]. In addition, mitochondrial dysfunction may be the
target of therapeutic measures to treat diseases such as obesity and diabetes.
Mitochondrial Involvement in Cardiovascular Complications
Heart diseases are also a major issue around the globe. There are many factors which
are involved in cardiovascular diseases, these are an environmental and genetic factor. From studies, it is confirmed that oxidative stress is directly proportional to an
increased number of mtDNA. The heart can generate many reactive species in the
heart cells including cardiac myocytes, endothelial cells, and neutrophils. There are
many in vivo and in vitro researches available that documented that oxidative stress
has a high impact on reducing reactive species in the cells [6]. The reactive species
in the heart are generated when ETC complexes I and III get disrupted [42]. In
accordance with this, other mechanisms are also involved in damaging heart tissues
by producing reactive oxygen species, these are NADPH oxidase, xanthine oxidoreductase, or NOS. The increased reactive oxygen species decreases the antioxidant
capacity of cell and causes cell injury which results in an alteration in gene expression, damaging mtDNA and abnormality in the functioning of endothelial cells [6],
this results in failing heart muscle called myocardium [43]. Additionally, reactive
oxygen species activate contractile functions, activate enzymes and transcription
factors. Thus, the reactive oxygen species could be involved in cardiovascular
diseases.
Mitochondrial Involvement in Stroke
Stroke is the main cause of death in developing countries. There are many factors
that induce a stroke. They may be economical, physiological, or others. Among
these, oxidative stress is also the contributing factor which causes a stroke by tissue
G. Murtaza et al.