Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress
Background/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardia...
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Format: | Article |
Language: | English |
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Karger Publishers
2015-02-01
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Series: | Kidney & Blood Pressure Research |
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Online Access: | http://www.karger.com/Article/FullText/368481 |
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author | Yingying Sun Tong Zhang Li Li Ji Wang |
author_facet | Yingying Sun Tong Zhang Li Li Ji Wang |
author_sort | Yingying Sun |
collection | DOAJ |
description | Background/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardiac hypertrophy to diastolic heart failure due to hypertension. Methods: We used spontaneously hypertensive rats (SHRs) to investigate possible signalling pathways for ER stress. Results: We found that cardiac protein and mRNA levels of glucose-regulated protein 78 were up-regulated. In addition, the CHOP- and caspase-12-dependent pathways, but not that of JNK, were activated in the SHR rats. Conclusions: These results suggest that ER stress can contribute to myocardial apoptosis during hypertensive disease. |
first_indexed | 2024-12-14T10:05:07Z |
format | Article |
id | doaj.art-0c6b801d2d08434abe05cd6745862b69 |
institution | Directory Open Access Journal |
issn | 1420-4096 1423-0143 |
language | English |
last_indexed | 2024-12-14T10:05:07Z |
publishDate | 2015-02-01 |
publisher | Karger Publishers |
record_format | Article |
series | Kidney & Blood Pressure Research |
spelling | doaj.art-0c6b801d2d08434abe05cd6745862b692022-12-21T23:07:09ZengKarger PublishersKidney & Blood Pressure Research1420-40961423-01432015-02-01401415110.1159/000368481368481Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum StressYingying SunTong ZhangLi LiJi WangBackground/Aims: Endoplasmic reticulum (ER) stress is one of the intrinsic apoptosis pathways, and cardiac apoptosis can occur in cardiovascular diseases, such as hypertension. However, the mechanisms by which ER stress leads to apoptosis remain enigmatic, particularly in the progression from cardiac hypertrophy to diastolic heart failure due to hypertension. Methods: We used spontaneously hypertensive rats (SHRs) to investigate possible signalling pathways for ER stress. Results: We found that cardiac protein and mRNA levels of glucose-regulated protein 78 were up-regulated. In addition, the CHOP- and caspase-12-dependent pathways, but not that of JNK, were activated in the SHR rats. Conclusions: These results suggest that ER stress can contribute to myocardial apoptosis during hypertensive disease.http://www.karger.com/Article/FullText/368481ApoptosisCaspase-12CHOPER stressGRP78Hypertension |
spellingShingle | Yingying Sun Tong Zhang Li Li Ji Wang Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress Kidney & Blood Pressure Research Apoptosis Caspase-12 CHOP ER stress GRP78 Hypertension |
title | Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress |
title_full | Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress |
title_fullStr | Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress |
title_full_unstemmed | Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress |
title_short | Induction of Apoptosis by Hypertension Via Endoplasmic Reticulum Stress |
title_sort | induction of apoptosis by hypertension via endoplasmic reticulum stress |
topic | Apoptosis Caspase-12 CHOP ER stress GRP78 Hypertension |
url | http://www.karger.com/Article/FullText/368481 |
work_keys_str_mv | AT yingyingsun inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress AT tongzhang inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress AT lili inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress AT jiwang inductionofapoptosisbyhypertensionviaendoplasmicreticulumstress |