Carvedilol promotes mitochondrial biogenesis by regulating the PGC-1/TFAM pathway in human umbilical vein endothelial cells (HUVECs)

Yao, Kai; Zhang, Wayne W.; Yao, Luyu; Yang, Shu; Nie, Wei; Huang, Feizhou

doi:10.1016/j.bbrc.2016.01.089

Cited by 49 publications

(38 citation statements)

References 17 publications

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“…However, our preliminary data exclude a modified ROS level in ren(2‐9) cells under basal conditions (data not shown). In other studies, enhanced MitoTracker red fluorescence intensity was associated with a hyperfusion of mitochondria or an increase of mitochondrial mass . From our analyses, we conclude that the enhanced MitoTracker red FLI in ren(2‐9) cells was not influenced by an altered mitochondrial mass but could be due to a shift of mitochondria away from the nucleus.…”

Section: Discussionsupporting

confidence: 64%

“…In other studies, enhanced MitoTracker red fluorescence intensity was associated with a hyperfusion of mitochondria 28 or an increase of mitochondrial mass. 29 From our analyses, we conclude that the enhanced MitoTracker red FLI in ren(2-9) cells was not influenced by an altered mitochondrial mass but could be due to a shift of mitochondria away from the nucleus. However, because nonyl-acridine orange labelling was subjected to a marked quenching effect, additional studies are necessary to verify this observation.…”

Section: Discussionmentioning

confidence: 56%

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An alternative renin isoform is cardioprotective by modulating mitochondrial metabolism

Wanka

Lutze

Staar

et al. 2018

J Cellular Molecular Medi

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The renin‐angiotensin system promotes oxidative stress, apoptosis, necrosis, fibrosis, and thus heart failure. Secretory renin plays a central role in these processes, initiating the generation of angiotensins. Nevertheless, alternative renin transcripts exist, which code for a cytosolically localized renin isoform (cyto‐renin) that is cardioprotective. We tested the hypothesis that the protective effects are associated with a beneficial switch of metabolic and mitochondrial functions. To assess H9c2 cell mitochondrial parameters, we used the Seahorse XF analyser. Cardiac H9c2 cells overexpressing cyto‐renin exhibited enhanced nonmitochondrial oxygen consumption, lactate accumulation, and LDH activity, reflecting a switch to more aerobic glycolysis known as Warburg effect. Additionally, mitochondrial spare capacity and cell respiratory control ratio were enhanced, indicating an increased potential to tolerate stress conditions. Renin knockdown induced opposite effects on mitochondrial functions without influencing metabolic parameters. Thus, the protective effects of cyto‐renin are associated with an altered bioenergetic profile and an enhanced stress tolerance, which are favourable under ischaemic conditions. Therefore, cyto‐renin is a promising new target for the prevention of ischaemia‐induced myocardial damage.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 56%

An alternative renin isoform is cardioprotective by modulating mitochondrial metabolism

Wanka

Lutze

Staar

et al. 2018

J Cellular Molecular Medi

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“…Figure 6 illustrates that the PGC1a promoter and ERRa response element activity were significantly and dose-dependently increased by gromwell root extract. To confirm that the increased PGC1a promoter activity led to changes in gene expression, PGC1a mRNA levels were measured in HepG2 cells and in HUVECs (a frequently used model to study PGC1a gene expression and mitochondria biogenesis) (29)(30)(31). PGC1a gene expression was dose-dependently increased in both HepG2 cells (Figure 7A-7C) and HUVECs ( Figure 7D-7 F), which mirrored the promoter activity data.…”

Section: Obesitysupporting

confidence: 65%

Lithospermum erythrorhizon Root and its Naphthoquinones Repress SREBP1c and Activate PGC1α Through AMPKα

Velliquette

Rajgopal

Rebhun

et al. 2017

Obesity

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Objective: To examine specific molecular mechanisms involved in modulating hepatic lipogenesis and mitochondria biogenesis signals by Lithospermum erythrorhizon (gromwell) root extract. Methods: Stable cell lines with luciferase reporter constructs were generated to examine sterol regulatory element binding protein 1c (SREBP1c) and peroxisome proliferator-activated receptor gamma, coactivator 1 (PGC1) a promoter activity and estrogen-related receptor (ERR) a response element activity. Gene expression of SREBP1c, stearoyl coenzyme A desaturase 1, and PGC1a was measured by using reverse transcription polymerase chain reaction. Lipogenesis was measured in human hepatoma cells with Nile red staining and flow cytometry. Phosphorylation of AMP-activated protein kinase (AMPK) a was determined by using ELISA and Western blot. Results: Gromwell root extract and its naphthoquinones dose-dependently repressed high glucose and liver X receptor a induction of SREBP1c promoter activity and gene expression. Hepatic lipogenesis was repressed, and PGC1a promoter and gene expression and ERRa response element activity were increased by gromwell root extract. Gromwell root extract, shikonin, and a-methyl-n-butyrylshikonin increased AMPKa phosphorylation, and inhibition of AMPK blunted the repression in SREBP1c promoter activity by gromwell root extract and its naphthoquinones. Conclusions: Data suggest that gromwell root extract and its naphthoquinones repress lipogenesis by increasing the phosphorylated state of AMPKa and stimulating mitochondrial biogenesis signals.

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“…; Yao et al. ). The effects of ACE inhibitor therapy on mitochondrial function are not clear: some studies demonstrating a protective effect from physiologic insult (e.g., myocardial infarction) (Hiona et al.…”

Section: Discussionmentioning

confidence: 98%

“…Also, several participants with BTHS were taking cardiac supportive care therapy including beta-blockers, ACE inhibitors and cardiac glycosides. Beta-blocker therapy appears to improve mitochondrial function through increase mitochondrial biogenesis and protection from oxidative stress (Gomez et al 2014;Sgobbo et al 2007;Yao et al 2016). The effects of ACE inhibitor therapy on mitochondrial function are not clear: some studies demonstrating a protective effect from physiologic insult (e.g., myocardial infarction) (Hiona et al 2011;Zoll et al 2006) where other report no significant effect on mitochondrial function, exercise capacity, or protection from insult (Bahi et al 2004;Thaveau et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Impaired cardiac and skeletal muscle bioenergetics in children, adolescents, and young adults with Barth syndrome

Bashir

Bohnert

Reeds

et al. 2017

Physiological Reports

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Barth syndrome (BTHS) is an X‐linked condition characterized by altered cardiolipin metabolism and cardioskeletal myopathy. We sought to compare cardiac and skeletal muscle bioenergetics in children, adolescents, and young adults with BTHS and unaffected controls and examine their relationships with cardiac function and exercise capacity. Children/adolescents and young adults with BTHS (n = 20) and children/adolescent and young adult control participants (n = 23, total n = 43) underwent 31P magnetic resonance spectroscopy (31P‐MRS) of the lower extremity (calf) and heart for estimation of skeletal muscle and cardiac bioenergetics. Peak exercise testing (VO 2peak) and resting echocardiography were also performed on all participants. Cardiac PCr/ATP ratio was significantly lower in children/adolescents (BTHS: 1.5 ± 0.2 vs. Control: 2.0 ± 0.3, P < 0.01) and adults (BTHS: 1.9 ± 0.2 vs. Control: 2.3 ± 0.2, P < 0.01) with BTHS compared to Control groups. Adults (BTHS: 76.4 ± 31.6 vs. Control: 35.0 ± 7.4 sec, P < 0.01) and children/adolescents (BTHS: 71.5 ± 21.3 vs. Control: 31.4 ± 7.4 sec, P < 0.01) with BTHS had significantly longer calf PCr recovery (τ PCr) postexercise compared to controls. Maximal calf ATP production through oxidative phosphorylation (Qmax‐lin) was significantly lower in children/adolescents (BTHS: 0.5 ± 0.1 vs. Control: 1.1 ± 0.3 mmol/L per sec, P < 0.01) and adults (BTHS: 0.5 ± 0.2 vs. Control: 1.0 ± 0.2 mmol/L sec, P < 0.01) with BTHS compared to controls. Blunted cardiac and skeletal muscle bioenergetics were associated with lower VO2peak but not resting cardiac function. Cardiac and skeletal muscle bioenergetics are impaired and appear to contribute to exercise intolerance in BTHS.

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Carvedilol promotes mitochondrial biogenesis by regulating the PGC-1/TFAM pathway in human umbilical vein endothelial cells (HUVECs)

Cited by 49 publications

References 17 publications

An alternative renin isoform is cardioprotective by modulating mitochondrial metabolism

An alternative renin isoform is cardioprotective by modulating mitochondrial metabolism

Lithospermum erythrorhizon Root and its Naphthoquinones Repress SREBP1c and Activate PGC1α Through AMPKα

Impaired cardiac and skeletal muscle bioenergetics in children, adolescents, and young adults with Barth syndrome

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