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mybpc3 ko pdk 4  (MedChemExpress)


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    MedChemExpress mybpc3 ko pdk 4
    A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and <t>Mybpc3</t> −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice <t>PDK4‐IN‐1</t> treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.
    Mybpc3 Ko Pdk 4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mybpc3 ko pdk 4/product/MedChemExpress
    Average 94 stars, based on 6 article reviews
    mybpc3 ko pdk 4 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure"

    Article Title: Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.125.041401

    A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and Mybpc3 −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice PDK4‐IN‐1 treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.
    Figure Legend Snippet: A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and Mybpc3 −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice PDK4‐IN‐1 treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Techniques Used: Labeling, Knock-Out, MANN-WHITNEY

    A , Immunohistochemical images and statistical analysis of the expression of PDK4 in Mybpc3 −/− mice at 2, 3, and 4 weeks. Scale bars represented 50 μm. B , The immunostaining of ACTN2 and PDK4 in different groups of human patients. C , The experimental design to construct conditional knockout of cardiac Pdk4 in Mybpc3 ‐KO mice. Pdk4 f/f ; Myh6‐Cre mice were generated through the crossbreeding of Pdk f/f mice with Myh6‐Cre transgenic mice. D , The identification of genotypes in different groups. E , Statistical analysis of the body weight of 3 groups. F , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and size of left ventricle. G , Representative Masson trichrome staining images illustrating fibrosis in Mybpc3 ‐KO and Pdk4 ‐CKO mice. Statistical analysis shows significant reduction in fibrosis in Pdk4 ‐CKO mice. H , Representative immunofluorescence staining images and quantitative analysis showing the expression levels of ACTN2 and PDK4 in different groups of mice: WT, Mybpc3 −/− , and Mybpc3 −/− / Pdk4 f/f ; Myh6‐Cre ; scale bars represent 20 μm. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. ACTN2 indicates actinin alpha 2; CKO, conditional knockout; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; ns, not significant; PDK4, pyruvate dehydrogenase kinase 4; Pdk4 ‐CKO, Pdk4 conditional knockout mice; and WT, wild type.
    Figure Legend Snippet: A , Immunohistochemical images and statistical analysis of the expression of PDK4 in Mybpc3 −/− mice at 2, 3, and 4 weeks. Scale bars represented 50 μm. B , The immunostaining of ACTN2 and PDK4 in different groups of human patients. C , The experimental design to construct conditional knockout of cardiac Pdk4 in Mybpc3 ‐KO mice. Pdk4 f/f ; Myh6‐Cre mice were generated through the crossbreeding of Pdk f/f mice with Myh6‐Cre transgenic mice. D , The identification of genotypes in different groups. E , Statistical analysis of the body weight of 3 groups. F , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and size of left ventricle. G , Representative Masson trichrome staining images illustrating fibrosis in Mybpc3 ‐KO and Pdk4 ‐CKO mice. Statistical analysis shows significant reduction in fibrosis in Pdk4 ‐CKO mice. H , Representative immunofluorescence staining images and quantitative analysis showing the expression levels of ACTN2 and PDK4 in different groups of mice: WT, Mybpc3 −/− , and Mybpc3 −/− / Pdk4 f/f ; Myh6‐Cre ; scale bars represent 20 μm. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. ACTN2 indicates actinin alpha 2; CKO, conditional knockout; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; ns, not significant; PDK4, pyruvate dehydrogenase kinase 4; Pdk4 ‐CKO, Pdk4 conditional knockout mice; and WT, wild type.

    Techniques Used: Immunohistochemical staining, Expressing, Immunostaining, Construct, Knock-Out, Generated, Transgenic Assay, Staining, Immunofluorescence, Double Knockout

    A , The experimental design to evaluate the effect of PDK4‐IN‐1 on Mybpc3 ‐KO mice. B , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and thickness of left ventricle. C , The heart from 3 groups and statistical analysis of heart weight. D , The representative Masson trichrome staining images and statistical analysis. E , The immunostaining of ACTN2 and PDK4 in different groups of mice (n WT =6, n Mybpc3 ‐KO =7, n Mybpc3 ‐KO+PDK4‐IN‐1 =7). Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. ACTN2 indicates actinin alpha 2; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; ns, not significant; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.
    Figure Legend Snippet: A , The experimental design to evaluate the effect of PDK4‐IN‐1 on Mybpc3 ‐KO mice. B , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and thickness of left ventricle. C , The heart from 3 groups and statistical analysis of heart weight. D , The representative Masson trichrome staining images and statistical analysis. E , The immunostaining of ACTN2 and PDK4 in different groups of mice (n WT =6, n Mybpc3 ‐KO =7, n Mybpc3 ‐KO+PDK4‐IN‐1 =7). Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. ACTN2 indicates actinin alpha 2; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; ns, not significant; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Techniques Used: Staining, Immunostaining, Knock-Out

    A , Schematic of the experiments procedure in 4 groups of mice: (1) PDK4‐CKO 4W: intragastric administration of PBS in PDK4‐CKO mice once every 2 days from 2W to 4W; (2) Mybpc3 ‐KO 8W+PDK4‐IN‐1: intragastric administration of PDK4‐IN‐1 in Mybpc3‐KO mice once every 2 days from 6W to 8W; (3) Mybpc3‐KO/Pdk4‐CKO 8W: intragastric administration of PBS in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W; (4) Mybpc3 ‐KO/ Pdk4 ‐CKO 8W+Tamoxifen: intragastric administration of tamoxifen in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W. B , M mode echocardiography of mice in each group. C , Statistics of EF of each group. D , H&E and Masson trichrome staining of mice in different treated groups (n=3). E , Quantification of ventricular fibrosis. F , Statistics of HW to BW ratio (HW/BW). G , TEM images of cardiac tissue in each group. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. BW indicates body weight; CKO, conditional knockout; EF, ejection fraction; H&E, hematoxylin and eosin; HW, heart weight; ns, not significant; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; PDK4, pyruvate dehydrogenase kinase 4; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and TEM, transmission electron microscopy.
    Figure Legend Snippet: A , Schematic of the experiments procedure in 4 groups of mice: (1) PDK4‐CKO 4W: intragastric administration of PBS in PDK4‐CKO mice once every 2 days from 2W to 4W; (2) Mybpc3 ‐KO 8W+PDK4‐IN‐1: intragastric administration of PDK4‐IN‐1 in Mybpc3‐KO mice once every 2 days from 6W to 8W; (3) Mybpc3‐KO/Pdk4‐CKO 8W: intragastric administration of PBS in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W; (4) Mybpc3 ‐KO/ Pdk4 ‐CKO 8W+Tamoxifen: intragastric administration of tamoxifen in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W. B , M mode echocardiography of mice in each group. C , Statistics of EF of each group. D , H&E and Masson trichrome staining of mice in different treated groups (n=3). E , Quantification of ventricular fibrosis. F , Statistics of HW to BW ratio (HW/BW). G , TEM images of cardiac tissue in each group. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. BW indicates body weight; CKO, conditional knockout; EF, ejection fraction; H&E, hematoxylin and eosin; HW, heart weight; ns, not significant; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; PDK4, pyruvate dehydrogenase kinase 4; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and TEM, transmission electron microscopy.

    Techniques Used: Staining, Knock-Out, Double Knockout, Transmission Assay, Electron Microscopy



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    mybpc3 ko pdk 4  (MedChemExpress)
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    MedChemExpress mybpc3 ko pdk 4
    A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and <t>Mybpc3</t> −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice <t>PDK4‐IN‐1</t> treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.
    Mybpc3 Ko Pdk 4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mybpc3 ko pdk 4/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    mybpc3 ko pdk 4 - by Bioz Stars, 2026-02
    94/100 stars
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    Image Search Results


    A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and Mybpc3 −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice PDK4‐IN‐1 treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure

    doi: 10.1161/JAHA.125.041401

    Figure Lengend Snippet: A , Metabolism of 13 C 6 ‐glucose. Horizontal columns indicate the fraction labeled in labeled metabolites in the WT and Mybpc3 −/− mice, total labeling of each metabolite normalized to 13 C 6 ‐glucose. B , The experimental design of Seahorse analysis. C , OCR was measured by Seahorse analysis with the indicated reagents in cardiomyocytes slices from Mybpc3‐KO (6‐week‐old) mice with PBS or pyruvate dehydrogenase kinase 4 inhibitor treatment. D , Basal respiration and glucose oxidation dependency were decreased in knockout mice PDK4‐IN‐1 treatment compared with PBS treatment. The glucose oxidation dependency measured by Seahorse XFe24 analyzer as described in the “ ” section. Statistical significance was calculated by Mann–Whitney U test. * P <0.05. Acetyl‐CoA indicates acetyl‐coenzyme A; BPTES, bis‐2‐(5‐phenylacetamido‐1,3,4‐thiadiazol‐2‐yl)ethyl sulfide; ETO, etomoxir; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; OCR, oxygen consumption rate; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Article Snippet: Mice in the Mybpc3 ‐KO+PDK4‐IN‐1 group were administered PDK4‐IN‐1 (100 mg/kg, MedChem Express, HY‐135954A) dissolved in PBS via intragastric injection.

    Techniques: Labeling, Knock-Out, MANN-WHITNEY

    A , Immunohistochemical images and statistical analysis of the expression of PDK4 in Mybpc3 −/− mice at 2, 3, and 4 weeks. Scale bars represented 50 μm. B , The immunostaining of ACTN2 and PDK4 in different groups of human patients. C , The experimental design to construct conditional knockout of cardiac Pdk4 in Mybpc3 ‐KO mice. Pdk4 f/f ; Myh6‐Cre mice were generated through the crossbreeding of Pdk f/f mice with Myh6‐Cre transgenic mice. D , The identification of genotypes in different groups. E , Statistical analysis of the body weight of 3 groups. F , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and size of left ventricle. G , Representative Masson trichrome staining images illustrating fibrosis in Mybpc3 ‐KO and Pdk4 ‐CKO mice. Statistical analysis shows significant reduction in fibrosis in Pdk4 ‐CKO mice. H , Representative immunofluorescence staining images and quantitative analysis showing the expression levels of ACTN2 and PDK4 in different groups of mice: WT, Mybpc3 −/− , and Mybpc3 −/− / Pdk4 f/f ; Myh6‐Cre ; scale bars represent 20 μm. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. ACTN2 indicates actinin alpha 2; CKO, conditional knockout; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; ns, not significant; PDK4, pyruvate dehydrogenase kinase 4; Pdk4 ‐CKO, Pdk4 conditional knockout mice; and WT, wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure

    doi: 10.1161/JAHA.125.041401

    Figure Lengend Snippet: A , Immunohistochemical images and statistical analysis of the expression of PDK4 in Mybpc3 −/− mice at 2, 3, and 4 weeks. Scale bars represented 50 μm. B , The immunostaining of ACTN2 and PDK4 in different groups of human patients. C , The experimental design to construct conditional knockout of cardiac Pdk4 in Mybpc3 ‐KO mice. Pdk4 f/f ; Myh6‐Cre mice were generated through the crossbreeding of Pdk f/f mice with Myh6‐Cre transgenic mice. D , The identification of genotypes in different groups. E , Statistical analysis of the body weight of 3 groups. F , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and size of left ventricle. G , Representative Masson trichrome staining images illustrating fibrosis in Mybpc3 ‐KO and Pdk4 ‐CKO mice. Statistical analysis shows significant reduction in fibrosis in Pdk4 ‐CKO mice. H , Representative immunofluorescence staining images and quantitative analysis showing the expression levels of ACTN2 and PDK4 in different groups of mice: WT, Mybpc3 −/− , and Mybpc3 −/− / Pdk4 f/f ; Myh6‐Cre ; scale bars represent 20 μm. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. ACTN2 indicates actinin alpha 2; CKO, conditional knockout; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; ns, not significant; PDK4, pyruvate dehydrogenase kinase 4; Pdk4 ‐CKO, Pdk4 conditional knockout mice; and WT, wild type.

    Article Snippet: Mice in the Mybpc3 ‐KO+PDK4‐IN‐1 group were administered PDK4‐IN‐1 (100 mg/kg, MedChem Express, HY‐135954A) dissolved in PBS via intragastric injection.

    Techniques: Immunohistochemical staining, Expressing, Immunostaining, Construct, Knock-Out, Generated, Transgenic Assay, Staining, Immunofluorescence, Double Knockout

    A , The experimental design to evaluate the effect of PDK4‐IN‐1 on Mybpc3 ‐KO mice. B , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and thickness of left ventricle. C , The heart from 3 groups and statistical analysis of heart weight. D , The representative Masson trichrome staining images and statistical analysis. E , The immunostaining of ACTN2 and PDK4 in different groups of mice (n WT =6, n Mybpc3 ‐KO =7, n Mybpc3 ‐KO+PDK4‐IN‐1 =7). Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. ACTN2 indicates actinin alpha 2; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; ns, not significant; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure

    doi: 10.1161/JAHA.125.041401

    Figure Lengend Snippet: A , The experimental design to evaluate the effect of PDK4‐IN‐1 on Mybpc3 ‐KO mice. B , The representative short‐axis echocardiography images of different groups and statistical analysis of heart failure and thickness of left ventricle. C , The heart from 3 groups and statistical analysis of heart weight. D , The representative Masson trichrome staining images and statistical analysis. E , The immunostaining of ACTN2 and PDK4 in different groups of mice (n WT =6, n Mybpc3 ‐KO =7, n Mybpc3 ‐KO+PDK4‐IN‐1 =7). Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001, **** P <0.0001. ACTN2 indicates actinin alpha 2; EF, ejection fraction; KO, knockout; LVESD, left ventricular end‐systolic diameter; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; ns, not significant; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and WT, wild type.

    Article Snippet: Mice in the Mybpc3 ‐KO+PDK4‐IN‐1 group were administered PDK4‐IN‐1 (100 mg/kg, MedChem Express, HY‐135954A) dissolved in PBS via intragastric injection.

    Techniques: Staining, Immunostaining, Knock-Out

    A , Schematic of the experiments procedure in 4 groups of mice: (1) PDK4‐CKO 4W: intragastric administration of PBS in PDK4‐CKO mice once every 2 days from 2W to 4W; (2) Mybpc3 ‐KO 8W+PDK4‐IN‐1: intragastric administration of PDK4‐IN‐1 in Mybpc3‐KO mice once every 2 days from 6W to 8W; (3) Mybpc3‐KO/Pdk4‐CKO 8W: intragastric administration of PBS in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W; (4) Mybpc3 ‐KO/ Pdk4 ‐CKO 8W+Tamoxifen: intragastric administration of tamoxifen in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W. B , M mode echocardiography of mice in each group. C , Statistics of EF of each group. D , H&E and Masson trichrome staining of mice in different treated groups (n=3). E , Quantification of ventricular fibrosis. F , Statistics of HW to BW ratio (HW/BW). G , TEM images of cardiac tissue in each group. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. BW indicates body weight; CKO, conditional knockout; EF, ejection fraction; H&E, hematoxylin and eosin; HW, heart weight; ns, not significant; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; PDK4, pyruvate dehydrogenase kinase 4; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and TEM, transmission electron microscopy.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure

    doi: 10.1161/JAHA.125.041401

    Figure Lengend Snippet: A , Schematic of the experiments procedure in 4 groups of mice: (1) PDK4‐CKO 4W: intragastric administration of PBS in PDK4‐CKO mice once every 2 days from 2W to 4W; (2) Mybpc3 ‐KO 8W+PDK4‐IN‐1: intragastric administration of PDK4‐IN‐1 in Mybpc3‐KO mice once every 2 days from 6W to 8W; (3) Mybpc3‐KO/Pdk4‐CKO 8W: intragastric administration of PBS in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W; (4) Mybpc3 ‐KO/ Pdk4 ‐CKO 8W+Tamoxifen: intragastric administration of tamoxifen in Mybpc3 ‐KO/ Pdk4 ‐CKO mice once every 2 days from 6W to 8W. B , M mode echocardiography of mice in each group. C , Statistics of EF of each group. D , H&E and Masson trichrome staining of mice in different treated groups (n=3). E , Quantification of ventricular fibrosis. F , Statistics of HW to BW ratio (HW/BW). G , TEM images of cardiac tissue in each group. Data are represented as mean±SD. Statistical significance was calculated by Kruskal–Wallis test with Dunn correction, * P <0.05, ** P <0.01, *** P <0.001. BW indicates body weight; CKO, conditional knockout; EF, ejection fraction; H&E, hematoxylin and eosin; HW, heart weight; ns, not significant; KO, knockout; Mybpc3 ‐KO, Mybpc3 −/− knockout mice; Mybpc3 ‐KO/ Pdk4 ‐CKO, Mybpc3 and Pdk4 conditional double knockout mice; PDK4, pyruvate dehydrogenase kinase 4; PDK4‐IN‐1, pyruvate dehydrogenase kinase 4 inhibitor; and TEM, transmission electron microscopy.

    Article Snippet: Mice in the Mybpc3 ‐KO+PDK4‐IN‐1 group were administered PDK4‐IN‐1 (100 mg/kg, MedChem Express, HY‐135954A) dissolved in PBS via intragastric injection.

    Techniques: Staining, Knock-Out, Double Knockout, Transmission Assay, Electron Microscopy