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a . I Na density I-V curves, max I Na densities and steady-state activation curves at BL (n=10), scrambled βadp1 (scr1, n=6) and βadp1 (n=7) in paired cardiomyocytes. b . Time-to-peak and decay time of the IDS traces at BL, scr1 and βadp1. c . Time-to-peak and decay time of the peak traces at BL, scr1 and βadp1. d . Representative images of perinexus in paired cardiomyocytes and the quantified perinexal width (W p ) at BL (perinexi: n=32), scr1 (perinexi: n=31) and βadp1 (perinexi: n=27). e . Co-localization of <t>Cx43,</t> Nav1.5 <t>and</t> <t>β1/β1b</t> within IDs between paired cardiomyocytes. One-way ANOVA followed by Tukey correction for multiple comparison. * p <0.05;** p <0.001;**** p <0.00001; ns, not significant.
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a . I Na density I-V curves, max I Na densities and steady-state activation curves at BL (n=10), scrambled βadp1 (scr1, n=6) and βadp1 (n=7) in paired cardiomyocytes. b . Time-to-peak and decay time of the IDS traces at BL, scr1 and βadp1. c . Time-to-peak and decay time of the peak traces at BL, scr1 and βadp1. d . Representative images of perinexus in paired cardiomyocytes and the quantified perinexal width (W p ) at BL (perinexi: n=32), scr1 (perinexi: n=31) and βadp1 (perinexi: n=27). e . Co-localization of <t>Cx43,</t> Nav1.5 <t>and</t> <t>β1/β1b</t> within IDs between paired cardiomyocytes. One-way ANOVA followed by Tukey correction for multiple comparison. * p <0.05;** p <0.001;**** p <0.00001; ns, not significant.
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Image Search Results


Molecular targets in cardiac remodeling by BiVP and LBBP. Western blotting results of BNP, TGF-β, KCNIP2, SERCA2a, Cx43, ANKRD1 protein expression (A, C, E) in septum and LV lateral walls from NC, DHF, and BiVP and LBBP groups, and relative protein expression (B, D, F). Represented images and statistical data (G) of cardiac fibrosis detected using Masson's staining. † P < .05 between septal and lateral walls. Abbreviations as in

Journal: European Heart Journal

Article Title: Left bundle branch vs biventricular pacing: mechanistic insights from a canine model

doi: 10.1093/eurheartj/ehaf1093

Figure Lengend Snippet: Molecular targets in cardiac remodeling by BiVP and LBBP. Western blotting results of BNP, TGF-β, KCNIP2, SERCA2a, Cx43, ANKRD1 protein expression (A, C, E) in septum and LV lateral walls from NC, DHF, and BiVP and LBBP groups, and relative protein expression (B, D, F). Represented images and statistical data (G) of cardiac fibrosis detected using Masson's staining. † P < .05 between septal and lateral walls. Abbreviations as in

Article Snippet: The levels of several key proteins were examined using western blot, including ANKRD1 (Proteintech, 11427-1-AP), BNP (Abclonal, A23996), Cx43 (Proteintech, 26980-1-AP), GSNOR (Proteintech, 66193-1-Ig), GLUD1 (Proteintech, 14299-1-AP), KCNIP2 (Abclonal, A7100), SERCA2a (Abclonal, A0098), TGF-β (Proteintech, 81746-2-RR), and GAPDH (Proteintech, 10494-1-AP).

Techniques: Western Blot, Expressing, Staining

Overview of the key findings. This study compares the treatment efficacy of LBBP and BiVP, and relating electrocardiographic, echocardiographic and cellular (reverse) remodeling in a canine DHF model. The results show that LBBP restores electrical synchrony (QRSd) to a similar extent as BiVP, while leads to larger LV-GLS improvement than BiVP. Both LBBP and BiVP reverse the protein level of KCNIP2, SERCA2a and Cx43. Moreover, LBBP reverses abnormalities in cytoskeleton-associated proteins, TGF-β signaling, and SERCA2a expression more than BiVP, as well as enhances myocardial energy metabolism via more efficient TCA cycling and ATP production. ANKRD1, ankyrin repeat domain 1; ATP, adenosine triphosphate; BiVP, biventricular pacing; BNP, B-type natriuretic peptide; Cx43, connexin 43; DHF dyssynchronous heart failure; ECG, electrocardiogram; echo, echocardiogram; GLUD1, glutamate dehydrogenase 1; GSNOR S-nitrosoglutathione reductase; KCNIP2, potassium voltage-gated channel interacting protein 2; LBBP, left bundle branch pacing; LV-GLS, left ventricular global longitudinal strain; NC, normal control; SERCA2a, sarcoplasmic/endoplasmic reticulum Ca 2+ ATPase 2a; TCA, tricarboxylic acid; TGF-β, Transforming growth factor-β.

Journal: European Heart Journal

Article Title: Left bundle branch vs biventricular pacing: mechanistic insights from a canine model

doi: 10.1093/eurheartj/ehaf1093

Figure Lengend Snippet: Overview of the key findings. This study compares the treatment efficacy of LBBP and BiVP, and relating electrocardiographic, echocardiographic and cellular (reverse) remodeling in a canine DHF model. The results show that LBBP restores electrical synchrony (QRSd) to a similar extent as BiVP, while leads to larger LV-GLS improvement than BiVP. Both LBBP and BiVP reverse the protein level of KCNIP2, SERCA2a and Cx43. Moreover, LBBP reverses abnormalities in cytoskeleton-associated proteins, TGF-β signaling, and SERCA2a expression more than BiVP, as well as enhances myocardial energy metabolism via more efficient TCA cycling and ATP production. ANKRD1, ankyrin repeat domain 1; ATP, adenosine triphosphate; BiVP, biventricular pacing; BNP, B-type natriuretic peptide; Cx43, connexin 43; DHF dyssynchronous heart failure; ECG, electrocardiogram; echo, echocardiogram; GLUD1, glutamate dehydrogenase 1; GSNOR S-nitrosoglutathione reductase; KCNIP2, potassium voltage-gated channel interacting protein 2; LBBP, left bundle branch pacing; LV-GLS, left ventricular global longitudinal strain; NC, normal control; SERCA2a, sarcoplasmic/endoplasmic reticulum Ca 2+ ATPase 2a; TCA, tricarboxylic acid; TGF-β, Transforming growth factor-β.

Article Snippet: The levels of several key proteins were examined using western blot, including ANKRD1 (Proteintech, 11427-1-AP), BNP (Abclonal, A23996), Cx43 (Proteintech, 26980-1-AP), GSNOR (Proteintech, 66193-1-Ig), GLUD1 (Proteintech, 14299-1-AP), KCNIP2 (Abclonal, A7100), SERCA2a (Abclonal, A0098), TGF-β (Proteintech, 81746-2-RR), and GAPDH (Proteintech, 10494-1-AP).

Techniques: Expressing, Control

a . I Na density I-V curves, max I Na densities and steady-state activation curves at BL (n=10), scrambled βadp1 (scr1, n=6) and βadp1 (n=7) in paired cardiomyocytes. b . Time-to-peak and decay time of the IDS traces at BL, scr1 and βadp1. c . Time-to-peak and decay time of the peak traces at BL, scr1 and βadp1. d . Representative images of perinexus in paired cardiomyocytes and the quantified perinexal width (W p ) at BL (perinexi: n=32), scr1 (perinexi: n=31) and βadp1 (perinexi: n=27). e . Co-localization of Cx43, Nav1.5 and β1/β1b within IDs between paired cardiomyocytes. One-way ANOVA followed by Tukey correction for multiple comparison. * p <0.05;** p <0.001;**** p <0.00001; ns, not significant.

Journal: bioRxiv

Article Title: Dissecting Gap Junctional and Ephaptic Contributions to Electrical Conduction in a Novel Cardiomyocyte Pair Model

doi: 10.64898/2026.03.05.709926

Figure Lengend Snippet: a . I Na density I-V curves, max I Na densities and steady-state activation curves at BL (n=10), scrambled βadp1 (scr1, n=6) and βadp1 (n=7) in paired cardiomyocytes. b . Time-to-peak and decay time of the IDS traces at BL, scr1 and βadp1. c . Time-to-peak and decay time of the peak traces at BL, scr1 and βadp1. d . Representative images of perinexus in paired cardiomyocytes and the quantified perinexal width (W p ) at BL (perinexi: n=32), scr1 (perinexi: n=31) and βadp1 (perinexi: n=27). e . Co-localization of Cx43, Nav1.5 and β1/β1b within IDs between paired cardiomyocytes. One-way ANOVA followed by Tukey correction for multiple comparison. * p <0.05;** p <0.001;**** p <0.00001; ns, not significant.

Article Snippet: Cardiomyocytes were labeled with a rabbit polyclonal antibody against either sodium channel Na v 1.5 (1:250, S0819, MilliporeSigma) or β1/β1b (1:200, Epitope: 44KRRSETTAETFTEWTFR60 , alongside with a mouse monoclonal antibody against Cx43 (1:250, sc-271837, Santa Cruz Biotechnology) and incubated at 4°C overnight.

Techniques: Activation Assay, Comparison