| Authors |
Cicalese SM, da Silva JF, Priviero F, Webb RC, Eguchi S, Tostes RC
|
| Submitted By |
Clinton Webb on 4/12/2021 |
| Status |
Published |
| Journal |
Circulation research |
| Year |
2021 |
| Date Published |
|
| Volume : Pages |
128 : 969 - 992 |
| PubMed Reference |
|
| Abstract |
Cells respond to stress by activating a variety of defense signaling pathways,
including cell survival and cell death pathways. Although cell survival
signaling helps the cell to recover from acute insults, cell death or senescence
pathways induced by chronic insults can lead to unresolved pathologies. Arterial
hypertension results from chronic physiological maladaptation against various
stressors represented by abnormal circulating or local neurohormonal factors,
mechanical stress, intracellular accumulation of toxic molecules, and
dysfunctional organelles. Hypertension and aging share common mechanisms that
mediate or prolong chronic cell stress, such as endoplasmic reticulum stress and
accumulation of protein aggregates, oxidative stress, metabolic mitochondrial
stress, DNA damage, stress-induced senescence, and proinflammatory processes.
This review discusses common adaptive signaling mechanisms against these
stresses including unfolded protein responses, antioxidant response element
signaling, autophagy, mitophagy, and mitochondrial fission/fusion, STING
(signaling effector stimulator of interferon genes)-mediated responses, and
activation of pattern recognition receptors. The main molecular mechanisms by
which the vasculature copes with hypertensive and aging stressors are presented
and recent advancements in stress-adaptive signaling mechanisms as well as
potential therapeutic targets are discussed.
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