IP3 receptors, stress and apoptosis

Lencesova, Lubomira; Krizanova, Olga

doi:10.4149/gpb_2012_014

Cited by 25Cell death mechanisms and regulationCalcium signaling and nucleotide metabolismIon channel regulation and function

IP3 receptors, stress and apoptosis

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Lencesova, Lubomira, Krizanova, Olga·2012·General physiology and biophysics

DOI 10.4149/gpb_2012_014

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Abstract

Inositol 1,4,5-trisphosphate (IP3) receptors are intracellular calcium channels that are able to release calcium from intracellular stores upon activation by IP3 and modulation by calcium. IP3 receptors are involved in variety of processes during physiological, but also in the pathophysiological states. Unraveling their regulation and function, especially under the pathological situations can result in a development of new therapeutic strategies based on the IP3 receptor´s activation and/or blocking. To the stimuli that can modulate IP3 receptors belong several stress factors (e.g. immobilization stress, oxidative stress and hypoxia) and also apoptosis. Depending on the length and strength of the stress stimulus, expression of IP3 receptors can be increased, or decreased. Therefore, in this minireview modulation of IP3 receptors by some stressors is discussed. Since it was already shown that strong hypoxia might lead to the apoptosis induction, special focus will be given to the hypoxic stress and induction of apoptosis.

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The increased BDNF and decreased caspase 3 may be induced by calcium overload of mitochondria with high levels of cAMP-calcium signaling.
“which may be induced by calcium overload of mitochondria with high levels of cAMP-calcium signaling”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Lencesova & Krizanova, 2012
The figure caption in the Conclusion (page unavailable) says that calcium transferred to mitochondria leads to activation of caspase 3, contrary to the claimed decrease. The “IP 3 receptors and apoptosis” section likewise links mitochondrial calcium accumulation to cell-death signaling. The passages found do not link this mechanism to increased BDNF or high cAMP-calcium signaling. (LLM, conf=0.84)
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Authors: Lencesova, L., & Krizanova, O.
Affiliations: Slovak Academy of Sciences (SK)
Venue: General physiology and biophysics
Publisher: AEPress, s.r.o.
Published: 2012
Volume: 31
Issue: 02
Pages: 119-130
ISSN: 0231-5882 (ISSN-L)
1338-4325
DOI: 10.4149/gpb_2012_014
OpenAlex: W2024527636
Cited by: 25
References: 106
Citations by year: 2026: 1 · 2025: 1 · 2023: 1 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 3
FWCI: 0.26
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: General Physiology and Biophysics (publishedVersion)
PubMed (publishedVersion)
Funders: Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Keywords: IP3 receptor, inositol 1,4,5-trisphosphate, intracellular calcium release, intracellular calcium stores, stress, apoptosis, hypoxia, oxidative stress, restraint stress, therapeutic targeting
MeSH terms: Animals, Calcium, Humans, Models, Biological, Ion Channel Gating, Apoptosis, Oxidative Stress, Calcium Signaling, Inositol 1,4,5-Trisphosphate Receptors

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