ArticleFrontiers in pharmacology2022
Kinin B1R Activation Induces Endoplasmic Reticulum Stress in Primary Hypothalamic Neurons.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Endoplasmic Reticulum Stress: A Novel Target for the Prevention and Treatment of Hypertension and Its Related Diseases.Journal of cellular and molecular medicine · 2025Review
- Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms.Circulation research · 2025Article
- Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice.Physiological reports · 2025Article
- Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Sodium formononetin-3'-sulphonate alleviates cerebral ischemia-reperfusion injury in rats via suppressing endoplasmic reticulum stress-mediated apoptosis.BMC neuroscience · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The endoplasmic reticulum (ER) is a key organelle involved in homeostatic functions including protein synthesis and transport, and the storage of free calcium. ER stress potentiates neuroinflammation and neurodegeneration and is a key contributor to the pathogenesis of neurogenic hypertension. Recently, we showed that kinin B1 receptor (B1R) activation plays a vital role in modulating neuroinflammation and hypertension. However, whether B1R activation results in the progression and enhancement of ER stress has not yet been studied. In this brief research report, we tested the hypothesis that B1R activation in neurons contributes to unfolded protein response (UPR) and the development of ER stress. To test this hypothesis, we treated primary hypothalamic neuronal cultures with B1R specific agonist Lys-Des-Arg
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