Heat shock transcription factor 1 regulates exercise‐induced myocardial angiogenesis after pressure overload via HIF‐1α/VEGF pathway

Tian, Xiaolin; Zhou, Ning; Yuan, Jie; Le, Lu Q.; Zhang, Qi; Wei, Minmin; Zou, Yunzeng; Yuan, Lingyan

doi:10.1111/jcmm.14872

Cited by 27 publications

(28 citation statements)

References 29 publications

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“…Several studies showed that HIF is activated under hypoxic conditions of different heart diseases such as ischemic heart disease or heart failure [ 81 ]. Morand et al demonstrated that chronic exposure to hypoxia induces ischemic ventricular arrhythmias and unexpected cardiac death [ 82 ].…”

Section: Dual Role Of Hypoxia In Acute and Chronic Disease Conditimentioning

confidence: 99%

Hypoxia and HIF Signaling: One Axis with Divergent Effects

Corrado

Fontana

2020

IJMS

135

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The correct concentration of oxygen in all tissues is a hallmark of cellular wellness, and the negative regulation of oxygen homeostasis is able to affect the cells and tissues of the whole organism. The cellular response to hypoxia is characterized by the activation of multiple genes involved in many biological processes. Among them, hypoxia-inducible factor (HIF) represents the master regulator of the hypoxia response. The active heterodimeric complex HIF α/β, binding to hypoxia-responsive elements (HREs), determines the induction of at least 100 target genes to restore tissue homeostasis. A growing body of evidence demonstrates that hypoxia signaling can act by generating contrasting responses in cells and tissues. Here, this dual and controversial role of hypoxia and the HIF signaling pathway is discussed, with particular reference to the effects induced on the complex activities of the immune system and on mechanisms determining cell and tissue responses after an injury in both acute and chronic human diseases related to the heart, lung, liver, and kidney.

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Section: Dual Role Of Hypoxia In Acute and Chronic Disease Conditimentioning

confidence: 99%

Hypoxia and HIF Signaling: One Axis with Divergent Effects

Corrado

Fontana

2020

IJMS

135

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“…Exercise-induced cardioprotection is underpinned by various molecular mechanisms, such as activation of heat shock and ER stress proteins as well as cyclooxygenase, enhancing the antioxidant capacity and autophagy processes [ 32 ]. Several studies investigated cardiac and skeletal muscle performance using mild to severe TAC with or without exercise in mice [ 8 , 18 ]. Studies on TAC and exercise intervention always applied exercise as secondary intervention.…”

Section: Discussionmentioning

confidence: 99%

“…The effect of exercise on HF development and associated muscle remodeling using the TAC model in mice was studied by Wang et al and Tian et al [ 8 , 18 ]. They observed improved cardiac performance following exercise training with increased intensity [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Structural and functional alterations in heart and skeletal muscle following severe TAC in mice: impact of moderate exercise training

et al. 2021

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Background Heart failure (HF) is the leading cause of death in western countries. Cardiac dysfunction is accompanied by skeletal alterations resulting in muscle weakness and fatigue. Exercise is an accepted interventional approach correcting cardiac and skeletal dysfunction, thereby improving mortality, re-hospitalization and quality of life. Animal models are used to characterize underpinning mechanisms. Transverse aortic constriction (TAC) results in cardiac pressure overload and finally HF. Whether exercise training improves cardiac remodeling and peripheral cachexia in the TAC mouse model was not analyzed yet. In this study, 2 weeks post TAC animals were randomized into two groups either performing a moderate exercise program (five times per week at 60% VO2 max for 40 min for a total of 8 weeks) or staying sedentary. Results In both TAC groups HF characteristics reduced ejection fraction (− 15% compared to sham, p < 0.001), cardiac remodeling (+ 22.5% cardiomyocyte cross sectional area compared to sham; p < 0.001) and coronary artery congestion (+ 34% diameter compared to sham; p = 0.008) were observed. Unexpectedly, peripheral cachexia was not detected. Furthermore, compared to sedentary group animals from the exercise group showed aggravated HF symptoms [heart area + 9% (p = 0.026), heart circumference + 7% (p = 0.002), right ventricular wall thickness − 30% (p = 0.003)] while muscle parameters were unchanged [Musculus soleus fiber diameter (p = 0.55), Musculus extensor digitorum longus contraction force (p = 0.90)]. Conclusion The severe TAC model is inappropriate to study moderate exercise effects in HF with respect to cardiac and skeletal muscle improvements. Further, the phenotype induced by different TAC procedures should be well documented and taken into account when planning experiments.

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“…In previous reports, it was found that HIF-1 α was an upstream signal factor for VEGF, and HIF-1 α could induce the VEGF expression [ 22 , 34 , 35 ]. However, in this clinical study, we did not find this relationship.…”

Section: Discussionmentioning

confidence: 99%

Association of Nuclear Receptor Coactivators with Hypoxia‐Inducible Factor‐1α in the Serum of Patients with Chronic Kidney Disease

Zhou

Lin

et al. 2020

BioMed Research International

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Nuclear receptor coactivators (NCOAs), consisting of coactivators and corepressors, dramatically enhance the transcriptional activity of nuclear receptors. Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that plays a major role under hypoxic conditions. This study was performed with the focus on the association of NCOAs with HIF-1α in the serum of chronic kidney disease (CKD) patients. Sixty patients with stage 5 CKD and 30 healthy controls from The Second Affiliated Hospital of Shantou University Medical College, between March 21, 2019, and October 30, 2019, were recruited in this prospective cohort study. We analyzed the serum levels of NCOAs (NCOA1, NCOA2, and NCOA3), HIF-1α, vascular endothelial growth factor (VEGF), etc. and assessed whether there was any relationship between these parameters and CKD disease. We found that circulating NCOA1 was positively associated with circulating NCOA2, NCOA3, and HIF-1α. A positive correlation was also observed between NCOA2 and NCOA1, NCOA3, HIF-1α, and VEGF. Furthermore, statistically significant correlations between NCOA3 and NCOA1, NCOA2, and HIF-1α were observed. The serum levels of VEGF in the CKD group were higher than those of the healthy control group. Circulating NCOA1 and circulating NCOA2 were negatively associated with procalcitonin. In conclusion, there was an association between circulating NCOA1, NCOA2, NCOA3, and circulating HIF-1α, and circulating VEGF was a risk factor for CKD disease. However, more studies should be performed to confirm this hypothesis.

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Heat shock transcription factor 1 regulates exercise‐induced myocardial angiogenesis after pressure overload via HIF‐1α/VEGF pathway

Cited by 27 publications

References 29 publications

Hypoxia and HIF Signaling: One Axis with Divergent Effects

Hypoxia and HIF Signaling: One Axis with Divergent Effects

Structural and functional alterations in heart and skeletal muscle following severe TAC in mice: impact of moderate exercise training

Association of Nuclear Receptor Coactivators with Hypoxia‐Inducible Factor‐1α in the Serum of Patients with Chronic Kidney Disease

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