Abstract
Aging is a process of irreversible decline in physiological function over the time. Several postulated mechanisms for aging include cumulative DNA damage, mitochondrial dysfunction, telomere loss, altered gene expression, and oxidative damages. Those factors affecting the aging process were implicated in hypertension, diabetes, lipid metabolic disorder, heart failure, smoking and psychological stress and so on. Subjects with those disorders are manifested the increased insulin resistance and oxidative stress which are more likely to accelerate aging, atherosclerosis and premature death. Both are also associated with accelerated telomere attrition in leucocytes and chronicle the cumulative burden of oxidative stress and inflammation over a life course. Here, recent evidences including our data about the relationship between telomere attrition and age-related disorders are introduced. Finally, we identify improving life-style as well as pharmacological interventions as potent anti-aging effects to be important for keeping of healthy long life.
| Original language | English |
|---|---|
| Pages (from-to) | 1332-1336 |
| Number of pages | 5 |
| Journal | Nippon rinsho. Japanese journal of clinical medicine |
| Volume | 67 |
| Issue number | 7 |
| Publication status | Published - Jan 1 2009 |
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All Science Journal Classification (ASJC) codes
- Medicine(all)
Cite this
Role of the environmental factors on aging. / Makino, Naoki; Maeda, Toyoki; Oyama, Junichi; Higuchi, Yoshihiro.
In: Nippon rinsho. Japanese journal of clinical medicine, Vol. 67, No. 7, 01.01.2009, p. 1332-1336.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Role of the environmental factors on aging
AU - Makino, Naoki
AU - Maeda, Toyoki
AU - Oyama, Junichi
AU - Higuchi, Yoshihiro
PY - 2009/1/1
Y1 - 2009/1/1
N2 - Aging is a process of irreversible decline in physiological function over the time. Several postulated mechanisms for aging include cumulative DNA damage, mitochondrial dysfunction, telomere loss, altered gene expression, and oxidative damages. Those factors affecting the aging process were implicated in hypertension, diabetes, lipid metabolic disorder, heart failure, smoking and psychological stress and so on. Subjects with those disorders are manifested the increased insulin resistance and oxidative stress which are more likely to accelerate aging, atherosclerosis and premature death. Both are also associated with accelerated telomere attrition in leucocytes and chronicle the cumulative burden of oxidative stress and inflammation over a life course. Here, recent evidences including our data about the relationship between telomere attrition and age-related disorders are introduced. Finally, we identify improving life-style as well as pharmacological interventions as potent anti-aging effects to be important for keeping of healthy long life.
AB - Aging is a process of irreversible decline in physiological function over the time. Several postulated mechanisms for aging include cumulative DNA damage, mitochondrial dysfunction, telomere loss, altered gene expression, and oxidative damages. Those factors affecting the aging process were implicated in hypertension, diabetes, lipid metabolic disorder, heart failure, smoking and psychological stress and so on. Subjects with those disorders are manifested the increased insulin resistance and oxidative stress which are more likely to accelerate aging, atherosclerosis and premature death. Both are also associated with accelerated telomere attrition in leucocytes and chronicle the cumulative burden of oxidative stress and inflammation over a life course. Here, recent evidences including our data about the relationship between telomere attrition and age-related disorders are introduced. Finally, we identify improving life-style as well as pharmacological interventions as potent anti-aging effects to be important for keeping of healthy long life.
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UR - http://www.scopus.com/inward/citedby.url?scp=69849097343&partnerID=8YFLogxK
M3 - Review article
C2 - 19591281
AN - SCOPUS:69849097343
VL - 67
SP - 1332
EP - 1336
JO - Astrophysical Journal
JF - Astrophysical Journal
SN - 0004-637X
IS - 7
ER -