Impact of cold adaptation on cardiac tolerance to ischemia-reperfusion. Role of glucocorticoid and thyroid hormones

Tsibulnikov, S. Yu.; Маслов, Л Н; Naryzhnaya, N. V.; Иванов, В. В.; Bushov, Yury; Воронков, Никита Сергеевич; Jaggi, Amteshwar Singh; Zhang, Yi; Oeltgen, Peter R.

doi:10.4149/gpb_2019002

Cited by 6 publications

(3 citation statements)

References 30 publications

(32 reference statements)

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“…It is known that adaptation to hypoxia and cold increases cardiac tolerance to I/R. 89,90 However, it is unknown whether reduced inflammation has a role in the infarct-reducing effect of adaptation.…”

Section: Conclusion and Clinical Perspectivementioning

confidence: 99%

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

Popov

Маслов

Naryzhnaya

et al. 2021

J Cardiovasc Pharmacol Ther

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While ischemia itself can kill heart muscle, much of the infarction after a transient period of coronary artery occlusion has been found to result from injury during reperfusion. Here we review the role of inflammation and possible pyroptosis in myocardial reperfusion injury. Current evidence suggests pyroptosis’s contribution to infarction may be considerable. Pyroptosis occurs when inflammasomes activate caspases that in turn cleave off an N-terminal fragment of gasdermin D. This active fragment makes large pores in the cell membrane thus killing the cell. Inhibition of inflammation enhances cardiac tolerance to ischemia and reperfusion injury. Stimulation of the purinergic P2X7 receptor and the β-adrenergic receptor and activation of nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) by toll-like receptor (TLR) agonists are all known to contribute to ischemia/reperfusion (I/R) cardiac injury through inflammation, potentially by pyroptosis. In contrast, stimulation of the cannabinoid CB2 receptor reduces I/R cardiac injury and inhibits this pathway. MicroRNAs, Akt, the phosphate and tension homology deleted on chromosome 10 protein (PTEN), pyruvate dehydrogenase and sirtuin-1 reportedly modulate inflammation in cardiomyocytes during I/R. Cryopyrin and caspase-1/4 inhibitors are reported to increase cardiac tolerance to ischemic and reperfusion cardiac injury, presumably by suppressing inflammasome-dependent inflammation. The ambiguity surrounding the role of pyroptosis in reperfusion injury arises because caspase-1 also activates cytotoxic interleukins and proteolytically degrades a surprisingly large number of cytosolic enzymes in addition to activating gasdermin D.

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Section: Conclusion and Clinical Perspectivementioning

confidence: 99%

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

Popov

Маслов

Naryzhnaya

et al. 2021

J Cardiovasc Pharmacol Ther

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“…28 It is possible that CRH and/or urocortin can be involved in the cardioprotective effect of chronic hypoxia or cold adaptation. 29 -31…”

Section: Crh and Urocortins In Stressmentioning

confidence: 99%

Cardioprotective and Vasoprotective Effects of Corticotropin-Releasing Hormone and Urocortins: Receptors and Signaling

Popov

Прокудина

Mukhomedzyanov

et al. 2021

J Cardiovasc Pharmacol Ther

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Despite the recent progress in research and therapy, cardiovascular diseases are still the most common cause of death worldwide, thus new approaches are still needed. The aim of this review is to highlight the cardioprotective potential of urocortins and corticotropin-releasing hormone (CRH) and their signaling. It has been documented that urocortins and CRH reduce ischemic and reperfusion (I/R) injury, prevent reperfusion ventricular tachycardia and fibrillation, and improve cardiac contractility during reperfusion. Urocortin-induced increase in cardiac tolerance to I/R depends mainly on the activation of corticotropin-releasing hormone receptor-2 (CRHR2) and its downstream pathways including tyrosine kinase Src, protein kinase A and C (PKA, PKCε) and extracellular signal-regulated kinase (ERK1/2). It was discussed the possibility of the involvement of interleukin-6, Janus kinase-2 and signal transducer and activator of transcription 3 (STAT3) and microRNAs in the cardioprotective effect of urocortins. Additionally, phospholipase-A2 inhibition, mitochondrial permeability transition pore (MPT-pore) blockade and suppression of apoptosis are involved in urocortin-elicited cardioprotection. Chronic administration of urocortin-2 prevents the development of postinfarction cardiac remodeling. Urocortin possesses vasoprotective and vasodilator effect; the former is mediated by PKC activation and prevents an impairment of endothelium-dependent coronary vasodilation after I/R in the isolated heart, while the latter includes both cAMP and cGMP signaling and its downstream targets. As CRHR2 is expressed by both cardiomyocytes and vascular endothelial cells. Urocortins mediate both endothelium-dependent and -independent relaxation of coronary arteries.

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“…New approaches are therefore needed to reduce myocardial infarct size and its severity. Recently, it was reported that cold acclimation (CA) possesses an infarct size-limiting effect (1,2). We have documented that exposure of rats to 5 wk of gradual mild cold acclimation (CA), followed by 2 wk of recovery resulted in reduction of myocardial infarct size without apparent side effects such as hypertension or hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

The cardioprotective effect persisting during recovery from cold acclimation is mediated by the β₂-adrenoceptor pathway and Akt activation

Tibenská

Marvanova

Elsnicová

et al. 2021

Journal of Applied Physiology

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The infarct size-limiting effect elicited by cold acclimation (CA) is accompanied by increased mitochondrial resistance and unaltered β1-adrenergic receptor (AR) signaling persisting for two weeks at room temperature. As the mechanism of CA-elicited cardioprotection is not fully understood we examined the role of the salvage β2-AR/Gi/Akt pathway. Male Wistar rats were exposed to CA (8 °C, 5 weeks), while the recovery group (CAR) was kept at 24 °C for additional 2 weeks. We show that the total number of myocardial β-ARs in the left ventricular myocardium did not change after CA but decreased after CAR. We confirmed the infarct size-limiting effect in both CA and CAR groups. Acute administration of β2-AR inhibitor ICI-118551 abolished the protective effect in the CAR group but had no effect in the control and CA groups. The inhibitory Giα1/2 and Giα3 proteins increased in the membrane fraction of the CAR group, and the p-AktSer473/Akt ratio also increased. Expression, phosphorylation, and mitochondrial location of the Akt target glycogen synthase kinase (GSK3β), were affected neither by CA nor by CAR. However, GSK3β translocated from the Z-disc to the H-zone after CA, and acquired its original location after CAR. Our data indicate that the cardioprotection observed after CAR is mediated by the β2-AR/Gi pathway and Akt activation. Further studies are needed to unravel downstream targets of the central regulators of the CA process and the downstream targets of the Akt protein after CAR.

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Impact of cold adaptation on cardiac tolerance to ischemia-reperfusion. Role of glucocorticoid and thyroid hormones

Cited by 6 publications

References 30 publications

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

Cardioprotective and Vasoprotective Effects of Corticotropin-Releasing Hormone and Urocortins: Receptors and Signaling

The cardioprotective effect persisting during recovery from cold acclimation is mediated by the β₂-adrenoceptor pathway and Akt activation

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Impact of cold adaptation on cardiac tolerance to ischemia-reperfusion. Role of glucocorticoid and thyroid hormones

Cited by 6 publications

References 30 publications

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

The Role of Pyroptosis in Ischemic and Reperfusion Injury of the Heart

Cardioprotective and Vasoprotective Effects of Corticotropin-Releasing Hormone and Urocortins: Receptors and Signaling

The cardioprotective effect persisting during recovery from cold acclimation is mediated by the β2-adrenoceptor pathway and Akt activation

Contact Info

Product

Resources

About

The cardioprotective effect persisting during recovery from cold acclimation is mediated by the β₂-adrenoceptor pathway and Akt activation