Hypoxia-Inducible Factor-1 Alpha in the Heart

Hashmi, Satwat; Al-Salam, Suhail

doi:10.1097/crd.0b013e31826287f6

Cited by 24 publications

(14 citation statements)

References 90 publications

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“…The most important factor that comes into play in cellular response to hypoxia is HIF-1α. It mediates the survival of injured cardiomyocytes in the setting of ischemic injury by transcribing a variety of cardioprotective genes including erythropoietin, vascular endothelial growth factor (VEGF), inducible nitric oxide synthase, hemeoxygenase-1, and cardiotropin [66]. GAL-3 has been linked to hypoxic/ischemic injuries in a number of studies in the kidneys and brain [43,58,59].…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Hashmi

Al-Salam

2015

Cardiovascular Pathology

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Section: Discussionmentioning

confidence: 99%

Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Hashmi

Al-Salam

2015

Cardiovascular Pathology

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“…Short-term induction of HIF-1 α is beneficial, as the injured myocardium metabolically adapts to hypoxic condition. 35 In contrast, long-term stabilization of HIF-1 α may be detrimental. 35, 36, 37, 38 Accordingly, we found that sustained hypoxic injury is followed by cardiomyoblast grief.…”

Section: Discussionmentioning

confidence: 99%

Agonist antibodies activating the Met receptor protect cardiomyoblasts from cobalt chloride-induced apoptosis and autophagy

et al. 2014

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Met, the tyrosine kinase receptor for hepatocyte growth factor (HGF), mainly activates prosurvival pathways, including protection from apoptosis. In this work, we investigated the cardioprotective mechanisms of Met activation by agonist monoclonal antibodies (mAbs). Cobalt chloride (CoCl2), a chemical mimetic of hypoxia, was used to induce cardiac damage in H9c2 cardiomyoblasts, which resulted in reduction of cell viability by (i) caspase-dependent apoptosis and (ii) – surprisingly – autophagy. Blocking either apoptosis with the caspase inhibitor benzyloxycarbonyl-VAD-fluoromethylketone or autophagosome formation with 3-methyladenine prevented loss of cell viability, which suggests that both processes contribute to cardiomyoblast injury. Concomitant treatment with Met-activating antibodies or HGF prevented apoptosis and autophagy. Pro-autophagic Redd1, Bnip3 and phospho-AMPK proteins, which are known to promote autophagy through inactivation of the mTOR pathway, were induced by CoCl2. Mechanistically, Met agonist antibodies or HGF prevented the inhibition of mTOR and reduced the flux of autophagosome formation. Accordingly, their anti-autophagic function was completely blunted by Temsirolimus, a specific mTOR inhibitor. Targeted Met activation was successful also in the setting of low oxygen conditions, in which Met agonist antibodies or HGF demonstrated anti-apoptotic and anti-autophagic effects. Activation of the Met pathway is thus a promising novel therapeutic tool for ischaemic injury.

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“…The highest level of HIF-1α protein is seen in the hypoxia group at 8000 m and hypoxia for 72 hours group. Hypoxia induces gradual upregulation of HIF-1α, which in turn induces the expression of adaptive genes erythropoiesis, vascular endothelial growth factor, glucose transporter-1, nitric oxide synthase (26,27). This means that there is an increase in HIF-1α protein level in hypoxic conditions and systemic adaptation occurs gradually at the cellular level in hypoxic conditions (27).…”

Section: Discussionmentioning

confidence: 99%

Effects of altitude and duration of different hypoxia exposure on HIF-1α in the rat brain, lung and heart tissues

Li¹,

Li²,

Tian³

et al. 2020

Preprint

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Objective: To explore the effects of hypoxic at different altitude and duration on the expression of HIF-1α in the rat tissues.Methods: A total of 72 Wistar rats were randomly divided into 6 groups (n=12 in each group): normoxic group and 5 experimental groups. Normoxia group was placed in the normal circumstances of Lanzhou (1500 m altitude), rats in the experimental groups were exposed to hypoxia in the hypobaric hypoxic animal experiment chamber simulating the altitudes of 3000, 4500, 6000, 7500, and 8000 m for 12 h, respectively. HE staining was conducted to observe the pathological changes of hippocampus tissues and the expression of HIF-1α in the rat brain, lung and heart tissues under the condition of hypoxia was detected by RT-PCR and Western Blotting. A total of 72 Wistar rats were randomly divided into 6 groups (n =12 in each group): normoxic group and 5 experimental groups.Rats in the experimental groups were exposed to hypoxia in the hypobaric hypoxic animal experiment chamber simulating the altitudes of 7500 m for 6, 12, 24, 36 and 72 h, respectively. Detect the same indicator after dissection.Results: We demonstrated that with the increased of hypoxia altitude and prolonged hypoxia, the expression of HIF-1α in the rat showed rising tendency (P<0.05) and the severe damage was revealed by pathological biopsy.Conclusion: We conclude that the expression of HIF1α in the rat was enslaved to the different altitude and duration of altitude hypoxia exposure.

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Hypoxia-Inducible Factor-1 Alpha in the Heart

Cited by 24 publications

References 90 publications

Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Galectin-3 is expressed in the myocardium very early post–myocardial infarction

Agonist antibodies activating the Met receptor protect cardiomyoblasts from cobalt chloride-induced apoptosis and autophagy

Effects of altitude and duration of different hypoxia exposure on HIF-1α in the rat brain, lung and heart tissues

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