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Induction of apoptosis by hypertension via endoplasmic reticulum stress

Yingying Sun, Tong Zhang, Li Li

    Kidney & Blood Pressure Research
    |March 21, 2015
    PubMed

    Insights

    Endoplasmic reticulum (ER) stress contributes to heart cell death in hypertension. This study found ER stress pathways, like CHOP and caspase-12, are activated in hypertensive rats, suggesting a role in cardiac apoptosis.

    Area of Science:

    • Cardiovascular Biology
    • Cellular Stress Response

    Background:

    • Endoplasmic reticulum (ER) stress is implicated in intrinsic apoptosis pathways.
    • Cardiac apoptosis is observed in cardiovascular diseases, including hypertension.
    • Mechanisms linking ER stress to apoptosis in hypertensive heart disease progression are not fully understood.

    Purpose of the Study:

    • Investigate signaling pathways involved in ER stress.
    • Elucidate the role of ER stress in the progression of hypertensive heart disease.

    Main Methods:

    • Utilized spontaneously hypertensive rats (SHRs) as a model system.
    • Examined cardiac protein and mRNA levels.
    • Assessed activation of specific signaling pathways.

    Main Results:

    • Increased cardiac protein and mRNA levels of glucose-regulated protein 78 were observed.
    • CHOP- and caspase-12-dependent pathways were activated in SHR rats.
    • JNK pathway activation was not detected in this model.

    Conclusions:

    • ER stress plays a role in myocardial apoptosis during hypertensive disease.
    • CHOP and caspase-12 are key mediators of ER stress-induced apoptosis in this context.
    Abstract

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