scholarly journals The Torpid State: Recent Advances in Metabolic Adaptations and Protective Mechanisms†

2021 ◽  
Vol 11 ◽  
Author(s):  
Sylvain Giroud ◽  
Caroline Habold ◽  
Roberto F. Nespolo ◽  
Carlos Mejías ◽  
Jérémy Terrien ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Adaptive Strategy ◽  
Resistance Mechanisms ◽  
Tropical Species ◽  
Special Focus ◽  
Protective Mechanisms ◽  
Origin And Evolution ◽  
Metabolic Adaptations ◽  
Central Organ ◽  
Molecular Aspects

Torpor and hibernation are powerful strategies enabling animals to survive periods of low resource availability. The state of torpor results from an active and drastic reduction of an individual’s metabolic rate (MR) associated with a relatively pronounced decrease in body temperature. To date, several forms of torpor have been described in all three mammalian subclasses, i.e., monotremes, marsupials, and placentals, as well as in a few avian orders. This review highlights some of the characteristics, from the whole organism down to cellular and molecular aspects, associated with the torpor phenotype. The first part of this review focuses on the specific metabolic adaptations of torpor, as it is used by many species from temperate zones. This notably includes the endocrine changes involved in fat- and food-storing hibernating species, explaining biomedical implications of MR depression. We further compare adaptive mechanisms occurring in opportunistic vs. seasonal heterotherms, such as tropical and sub-tropical species. Such comparisons bring new insights into the metabolic origins of hibernation among tropical species, including resistance mechanisms to oxidative stress. The second section of this review emphasizes the mechanisms enabling heterotherms to protect their key organs against potential threats, such as reactive oxygen species, associated with the torpid state. We notably address the mechanisms of cellular rehabilitation and protection during torpor and hibernation, with an emphasis on the brain, a central organ requiring protection during torpor and recovery. Also, a special focus is given to the role of an ubiquitous and readily-diffusing molecule, hydrogen sulfide (H2S), in protecting against ischemia-reperfusion damage in various organs over the torpor-arousal cycle and during the torpid state. We conclude that (i) the flexibility of torpor use as an adaptive strategy enables different heterothermic species to substantially suppress their energy needs during periods of severely reduced food availability, (ii) the torpor phenotype implies marked metabolic adaptations from the whole organism down to cellular and molecular levels, and (iii) the torpid state is associated with highly efficient rehabilitation and protective mechanisms ensuring the continuity of proper bodily functions. Comparison of mechanisms in monotremes and marsupials is warranted for understanding the origin and evolution of mammalian torpor.

scholarly journals Molecular Aspects of Volatile Anesthetic-Induced Organ Protection and Its Potential in Kidney Transplantation

2021 ◽  
Vol 22 (5) ◽  
pp. 2727
Author(s):  
Gertrude J. Nieuwenhuijs-Moeke ◽  
Dirk J. Bosch ◽  
Henri G.D. Leuvenink
Keyword(s):  
Kidney Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Animal Experiments ◽  
Volatile Anesthetic ◽  
Organ Protection ◽  
Graft Outcome ◽  
Molecular Aspects

Ischemia reperfusion injury (IRI) is inevitable in kidney transplantation and negatively impacts graft and patient outcome. Reperfusion takes place in the recipient and most of the injury following ischemia and reperfusion occurs during this reperfusion phase; therefore, the intra-operative period seems an attractive window of opportunity to modulate IRI and improve short- and potentially long-term graft outcome. Commonly used volatile anesthetics such as sevoflurane and isoflurane have been shown to interfere with many of the pathophysiological processes involved in the injurious cascade of IRI. Therefore, volatile anesthetic (VA) agents might be the preferred anesthetics used during the transplantation procedure. This review highlights the molecular and cellular protective points of engagement of VA shown in in vitro studies and in vivo animal experiments, and the potential translation of these results to the clinical setting of kidney transplantation.

scholarly journals Hepatic cell mobilization for protection against ischemic myocardial injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shu Q. Liu ◽  
John B. Troy ◽  
Chi-Hao Luan ◽  
Roger J. Guillory
Keyword(s):  
Ischemia Reperfusion ◽  
Hepatic Cell ◽  
Ischemic Myocardium ◽  
Cell Nuclei ◽  
Protective Mechanisms ◽  
Specific Expression ◽  
Time Points ◽  
Hepatic Cells ◽  
Cell Mobilization ◽  
Myocardial Ischemia Reperfusion

AbstractThe heart is capable of activating protective mechanisms in response to ischemic injury to support myocardial survival and performance. These mechanisms have been recognized primarily in the ischemic heart, involving paracrine signaling processes. Here, we report a distant cardioprotective mechanism involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardial ischemia–reperfusion (MI-R) injury. A parabiotic mouse model was generated by surgical skin-union of two mice and used to induce bilateral MI-R injury with unilateral hepatectomy, establishing concurrent gain- and loss-of-hepatic cell mobilization conditions. Hepatic cells, identified based on the cell-specific expression of enhanced YFP, were found in the ischemic myocardium of parabiotic mice with intact liver (0.2 ± 0.1%, 1.1 ± 0.3%, 2.7 ± 0.6, and 0.7 ± 0.4% at 1, 3, 5, and 10 days, respectively, in reference to the total cell nuclei), but not significantly in the ischemic myocardium of parabiotic mice with hepatectomy (0 ± 0%, 0.1 ± 0.1%, 0.3 ± 0.2%, and 0.08 ± 0.08% at the same time points). The mobilized hepatic cells were able to express and release trefoil factor 3 (TFF3), a protein mitigating MI-R injury as demonstrated in TFF3−/− mice (myocardium infarcts 17.6 ± 2.3%, 20.7 ± 2.6%, and 15.3 ± 3.8% at 1, 5, and 10 days, respectively) in reference to wildtype mice (11.7 ± 1.9%, 13.8 ± 2.3%, and 11.0 ± 1.8% at the same time points). These observations suggest that MI-R injury can induce hepatic cell mobilization to support myocardial survival by releasing TFF3.

scholarly journals Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Xia Yin ◽  
Yang Zheng ◽  
Xujie Zhai ◽  
Xin Zhao ◽  
Lu Cai
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Protective Effect ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Patients ◽  
Protective Mechanisms ◽  
Gsk 3Β ◽  
Pathogenic Effects

Ischemic preconditioning (IPC) or postconditioning (Ipost) is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.

scholarly journals Origin and Evolution of the Neuroendocrine Control of Reproduction in Vertebrates, With Special Focus on Genome and Gene Duplications

2020 ◽  
Vol 100 (2) ◽  
pp. 869-943 ◽  
Author(s):  
Sylvie Dufour ◽  
Bruno Quérat ◽  
Hervé Tostivint ◽  
Catherine Pasqualini ◽  
Hubert Vaudry ◽  
...  
Keyword(s):  
Special Focus ◽  
Gene Duplications ◽  
Vertebrate Lineage ◽  
Neuroendocrine Control ◽  
Origin And Evolution ◽  
Large Panel ◽  
Gonadotropic Axis ◽  
Duplication Events ◽  
The Brain ◽  
Hypophysial Portal

In humans, as in the other mammals, the neuroendocrine control of reproduction is ensured by the brain-pituitary gonadotropic axis. Multiple internal and environmental cues are integrated via brain neuronal networks, ultimately leading to the modulation of the activity of gonadotropin-releasing hormone (GnRH) neurons. The decapeptide GnRH is released into the hypothalamic-hypophysial portal blood system and stimulates the production of pituitary glycoprotein hormones, the two gonadotropins luteinizing hormone and follicle-stimulating hormone. A novel actor, the neuropeptide kisspeptin, acting upstream of GnRH, has attracted increasing attention in recent years. Other neuropeptides, such as gonadotropin-inhibiting hormone/RF-amide related peptide, and other members of the RF-amide peptide superfamily, as well as various nonpeptidic neuromediators such as dopamine and serotonin also provide a large panel of stimulatory or inhibitory regulators. This paper addresses the origin and evolution of the vertebrate gonadotropic axis. Brain-pituitary neuroendocrine axes are typical of vertebrates, the pituitary gland, mediator and amplifier of brain control on peripheral organs, being a vertebrate innovation. The paper reviews, from molecular and functional perspectives, the evolution across vertebrate radiation of some key actors of the vertebrate neuroendocrine control of reproduction and traces back their origin along the vertebrate lineage and in other metazoa before the emergence of vertebrates. A focus is given on how gene duplications, resulting from either local events or from whole genome duplication events, and followed by paralogous gene loss or conservation, might have shaped the evolutionary scenarios of current families of key actors of the gonadotropic axis.

scholarly journals Noninvasive approach to mend the broken heart: Is “remote conditioning” a promising strategy for application in humans?

2017 ◽  
Vol 95 (10) ◽  
pp. 1204-1212 ◽  
Author(s):  
Táňa Ravingerová ◽  
Veronika Farkašová ◽  
Lucia Griecsová ◽  
Martina Muráriková ◽  
Slavka Carnická ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cost Effective ◽  
Neural Pathways ◽  
Protective Mechanisms ◽  
Clinical Role ◽  
Technical Requirements ◽  
Promising Strategy ◽  
Remote Organ ◽  
Local Stimulus

Currently, there are no satisfactory interventions to protect the heart against the detrimental effects of ischemia–reperfusion injury. Although ischemic preconditioning (PC) is the most powerful form of intrinsic cardioprotection, its application in humans is limited to planned interventions, due to its short duration and technical requirements. However, many organs/tissues are capable of producing “remote” PC (RPC) when subjected to brief bouts of ischemia–reperfusion. RPC was first described in the heart where brief ischemia in one territory led to protection in other area. Later on, RPC started to be used in patients with acute myocardial infarction, albeit with ambiguous results. It is hypothesized that the connection between the signal triggered in remote organ and protection induced in the heart can be mediated by humoral and neural pathways, as well as via systemic response to short sublethal ischemia. However, although RPC has a potentially important clinical role, our understanding of the mechanistic pathways linking the local stimulus to the remote organ remains incomplete. Nevertheless, RPC appears as a cost-effective and easily performed intervention. Elucidation of protective mechanisms activated in the remote organ may have therapeutic and diagnostic implications in the management of myocardial ischemia and lead to development of pharmacological RPC mimetics.

scholarly journals Ischemic Postconditioning as a Novel Avenue to Protect against Brain Injury after Stroke

2009 ◽  
Vol 29 (5) ◽  
pp. 873-885 ◽  
Author(s):  
Heng Zhao
Keyword(s):  
Protein Kinase ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Protective Mechanisms ◽  
Mitogen Activated Protein ◽  
Cerebral Ischemic

Ischemic postconditioning initially referred to a stuttering reperfusion performed immediately after reperfusion, for preventing ischemia/reperfusion injury in both myocardial and cerebral infarction. It has evolved into a concept that can be induced by a broad range of stimuli or triggers, and may even be performed as late as 6 h after focal ischemia and 2 days after transient global ischemia. The concept is thought to be derived from ischemic preconditioning or partial/gradual reperfusion, but in fact the first experiment for postconditioning was carried out much earlier than that of preconditioning or partial/gradual reperfusion, in the research on myocardial ischemia. This review first examines the protective effects and parameters of postconditioning in various cerebral ischemic models. Thereafter, it provides insights into the protective mechanisms of postconditioning associated with reperfusion injury and the Akt, mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and ATP-sensitive K+ (KATP) channel cell signaling pathways. Finally, some open issues and future challenges regarding clinical translation of postconditioning are discussed.

scholarly journals Maize plants produce direct resistance elicited by Tetranychus urticae Koch (Acari: Tetranychidae)

2017 ◽  
Vol 78 (1) ◽  
pp. 13-17 ◽  
Author(s):  
P. D. Paulo ◽  
C. G. Lima ◽  
A. B. Dominiquini ◽  
M. A. M. Fadini ◽  
S. M. Mendes ◽  
...  
Keyword(s):  
Tetranychus Urticae ◽  
Spider Mite ◽  
Resistance Mechanisms ◽  
Adult Survival ◽  
Female Adult ◽  
Protective Mechanisms ◽  
Survival And Reproduction ◽  
Maize Plants ◽  
Two Spotted Spider Mite ◽  
Tetranychus Urticae Koch

Abstract Plants can be attacked by a wide variety of herbivores. Thus, developing protective mechanisms for resistance against these agents is an advantage for survival and reproduction. Over the course of evolution, many resistance mechanisms against herbivory have been developed by the plants. Induced direct and indirect resistance mechanisms can manifest in plants after herbivore attack. The two-spotted spider mite Tetranychus urticae is not a pest of maize crops (Zea mays), despite being reported infesting plants that may have resistances against this herbivore. We tested the hypothesis that maize plants would be able to induce direct resistance against T. urticae after, evaluating the effect of T. urticae infestation in maize plants on the development and reproduction of conspecifics. We tested induced direct resistance performing infestation and measuring biological parameters upon a second infestation. Maize plants, 40 days after sowing, were divided into two groups: 30 not infested by T. urticae (clean plants clean) and, 30 infested by the spider mite. Infestation of maize plants by T. urticae reduced the conspecific female adult survival. However, no change in the survival of immature or reproduction was observed. These results suggest the induction of induced direct resistances in maize by T. urticae. This is first report of direct resistance induction in Z. mays by the two-spotted spider mite T. urticae.

scholarly journals Akt Inhibition as Preconditioning Treatment to Protect Kidney Cells against Anoxia

2021 ◽  
Vol 23 (1) ◽  
pp. 152
Author(s):  
Nicolas Melis ◽  
Romain Carcy ◽  
Isabelle Rubera ◽  
Marc Cougnon ◽  
Christophe Duranton ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Oxygen Demand ◽  
Ischemic Tolerance ◽  
Kidney Cells ◽  
Protective Mechanisms ◽  
Akt Phosphorylation ◽  
Mitochondrial Ros ◽  
Highly Sensitive ◽  
High Oxygen Demand ◽  
Survival Effect

Lesions issued from the ischemia/reperfusion (I/R) stress are a major challenge in human pathophysiology. Of human organs, the kidney is highly sensitive to I/R because of its high oxygen demand and poor regenerative capacity. Previous studies have shown that targeting the hypusination pathway of eIF5A through GC7 greatly improves ischemic tolerance and can be applied successfully to kidney transplants. The protection process correlates with a metabolic shift from oxidative phosphorylation to glycolysis. Because the protein kinase B Akt is involved in ischemic protective mechanisms and glucose metabolism, we looked for a link between the effects of GC7 and Akt in proximal kidney cells exposed to anoxia or the mitotoxic myxothiazol. We found that GC7 treatment resulted in impaired Akt phosphorylation at the Ser473 and Thr308 sites, so the effects of direct Akt inhibition as a preconditioning protocol on ischemic tolerance were investigated. We evidenced that Akt inhibitors provide huge protection for kidney cells against ischemia and myxothiazol. The pro-survival effect of Akt inhibitors, which is reversible, implied a decrease in mitochondrial ROS production but was not related to metabolic changes or an antioxidant defense increase. Therefore, the inhibition of Akt can be considered as a preconditioning treatment against ischemia.

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