C/EBPβ is required in pregnancy-induced cardiac hypertrophy

Redondo-Angulo, Ibon; Mas‐Stachurska, Aleksandra; Sitges, Marta; Giralt, Marta; Villarroya, Francesc; Planavila, Anna

doi:10.1016/j.ijcard.2015.10.005

Cited by 16 publications

(8 citation statements)

References 38 publications

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“…8, 10, 26 In mouse hearts, a significant induction was found, consistent with our observations. 27 Thus, our data demonstrate not only clear induction of PDK4, but also that the induction is necessary for the substrate switch, since inhibition of PDK with DCA reverses the energetic changes of pregnancy (Figure 4F). …”

Section: Discussionsupporting

confidence: 51%

PDK4 Inhibits Cardiac Pyruvate Oxidation in Late Pregnancy

Liu

Rowe

Yang

et al. 2017

Circulation Research

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Rationale Pregnancy profoundly alters maternal physiology. The heart hypertrophies during pregnancy, but its metabolic adaptations are not well understood. Objective To determine the mechanisms underlying cardiac substrate use during pregnancy. Methods and Results We use here 13C-glucose, 13C-lactate, and 13C-fatty acid tracing analyses to show that hearts in late pregnant mice increase fatty acid uptake and oxidation into the tricarboxylic acid (TCA) cycle, while reducing glucose and lactate oxidation. Mitochondrial quantity, morphology, and function do not appear altered. Insulin signaling appears intact, and the abundance and localization of the major fatty acid and glucose transporters, CD36 and GLUT4, are also unchanged. Rather, we find that the pregnancy hormone progesterone induces pyruvate dehydrogenase kinase (PDK)-4 in cardiomyocytes, and that elevated PDK4 levels in late pregnancy lead to inhibition of pyruvate dehydrogenase (PDH) and pyruvate flux into the TCA cycle. Blocking PDK4 reverses the metabolic changes seen in hearts in late pregnancy. Conclusions Taken together, these data indicate that the hormonal environment of late pregnancy promotes metabolic remodeling in the heart at the level of PDH, rather than at the level of insulin signaling.

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Section: Discussionsupporting

confidence: 51%

PDK4 Inhibits Cardiac Pyruvate Oxidation in Late Pregnancy

Liu

Rowe

Yang

et al. 2017

Circulation Research

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“…4 e ). We found that cardiac Metrnβ overexpression up-regulated the transcript levels of these genes and, more important, that the ratio M1/M2 macrophages estimated on the basis of the iNOS / Arg1 ratio ( Redondo-Angulo et al, 2016 ; Cereijo et al, 2018 ) was significantly down-regulated in the hearts of Metrnβ-overexpressing mice ( Fig. 4 f ).…”

Section: Resultsmentioning

confidence: 75%

Meteorin-like/Meteorin-β protects heart against cardiac dysfunction

Rupérez

Ferrer-Curriu

Cervera-Barea

et al. 2021

Journal of Experimental Medicine

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Meteorin-like/Meteorin-β (Metrnl/Metrnβ) is a secreted protein produced by skeletal muscle and adipose tissue that exerts metabolic actions that improve glucose metabolism. The role of Metrnβ in cardiac disease is completely unknown. Here, we show that Metrnβ-null mice exhibit asymmetrical cardiac hypertrophy, fibrosis, and enhanced signs of cardiac dysfunction in response to isoproterenol-induced cardiac hypertrophy and aging. Conversely, adeno-associated virus–mediated specific overexpression of Metrnβ in the heart prevents the development of cardiac remodeling. Furthermore, Metrnβ inhibits cardiac hypertrophy development in cardiomyocytes in vitro, indicating a direct effect on cardiac cells. Antibody-mediated blockage of Metrnβ in cardiomyocyte cell cultures indicated an autocrine action of Metrnβ on the heart, in addition to an endocrine action. Moreover, Metrnβ is highly produced in the heart, and analysis of circulating Metrnβ concentrations in a large cohort of patients reveals that it is a new biomarker of heart failure with an independent prognostic value.

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“…Members from STEAP3 family exhibited different expressional profiles. STEAP1 and STEAP2 are highly expressed in the prostate gland, and was found to be closely associated with prostate cancer metastasis [31,47]. STEAP4 is highly expressed in adipose tissue and is a co-regulator of nutrients and inflammation [44].…”

Section: Discussionmentioning

confidence: 99%

ISCA1 Deficiency Induces Iron Metabolism Disorder and Myocardial Oncosis in Rat

Yang¹,

Yang²,

X³

et al. 2021

Preprint

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The effects of multiple mitochondrial dysfunction (MMD) on heart, a highly mitochondria-dependent tissue, is still unclear. This study was the first to verify the effect of ISCA1 gene deficiency, which has been shown to cause multiple mitochondrial dysfunction syndromes type 5 (MMDS5), on cardiac development in vivo, that is cardiomyocytes suffer from energy shortage due to abnormal metabolism of iron ion, which leads to oncosis and eventually HF and body death. Subsequently, we determine a new interacting molecule for ISCA1, six-transmembrane epithelial antigen of prostate 3 (STEAP3), which acts as a reductase in the reduction of Fe3+ to Fe2+. Forward and reverse validation experiments demonstrated that STEAP3 plays an important role in iron metabolism and energy generation impairment induced by ISCA1 deficiency. This result provides theoretical basis for understanding of MMDS pathogenesis, especially on heart development and the pathological process of heart diseases, and finally provides new clues for searching of clinical therapeutic targets.

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C/EBPβ is required in pregnancy-induced cardiac hypertrophy

Cited by 16 publications

References 38 publications

PDK4 Inhibits Cardiac Pyruvate Oxidation in Late Pregnancy

PDK4 Inhibits Cardiac Pyruvate Oxidation in Late Pregnancy

Meteorin-like/Meteorin-β protects heart against cardiac dysfunction

ISCA1 Deficiency Induces Iron Metabolism Disorder and Myocardial Oncosis in Rat

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