Table 3.
Gap Junction Remodeling in Left Ventricular Hypertrophy
| Reference | LVH Model | Finding |
|---|---|---|
| Kostin et al. 49 | Human aortic stenosis | 44.3% increase in Cx43 protein, augmented number of GJs per 100 μm2 intercalated disc, increased GJ surface density in compensated hypertrophy |
| Dimished and heterogenous Cx43 distribution in decompensated hypertrophy | ||
| Peters et al. 50 | Human aortic stenosis | Cx43 gap junction expression per myocyte not significantly different from normal, reduced by 40% per unit volume of myocyte |
| Dupont et al. 51 | Human cardiomyopathy with end‐stage heart failure | Reduced level of Cx43, spatially heterogeneous |
| Emdad et al. 52 | Aortic‐band rats 4–12 months after operation | Dispersion of punctuate Cx43 labeling over the entire cell surface, significantly decreased proportion of Cx43 label at the intercalated disk, reduction of Cx43 gap junctions in the intercalated disc center Cx43‐containing gap junctions displaced from the usual locations to form side‐to‐side contacts distant from the disk, also appearing as annual profiles |
| Wang and Gerdes 53 | Aortic stenosis in guinea pigs 4, 6 months after operation | No change at the compensated hypertrophy stage, a decrease in Cx43 per LV myocyte by 37% at the congestive heart failure stage |
| Peters et al. 54 | Renovascular hypertension in guinea pigs | In early phases — a substantially increased connexin43 gap junction expression compared to controls, both when measured per cell (increased by 45%) and per unit volume of myocyte (increase by 30%) |
| Okabe et al. 25 | SHR 15 w | Diminution of the number of step‐to‐step and side‐to‐side junctions |
| Tribulova et al. 55 | SHR 13 w | No differences in the overall density of myocardial gap junctions as compared to control WKY rats, a significant decrease in phosphorylated isoform of Cx43, a higher number of lateral, side‐to‐side connections |
| Bacharova et al. 56 | SHR 20 w | Lower values of Cx43 of about 40% as compared to Wistar normotensive rats, corresponding to lower values of QRSmax and SP of about 37 and 50%, respectively |
| Itoh et al. 57 | Arteriovenous shunt in rabbits 12 weeks after operation | Significant decrease in Cx43 mRNA expression 12 weeks after the shunt operation |
| Goldfine et al. 58 | Ao regurgitation in New Zealand white rabbits 1 month, ≥2.5 year after operation | Initial tendency of Cx43 expression in AR animals to be less than that of age‐matched controls (1 month), and its increase as in the ≥ 2.5 year AR animals |
| Formigli et al. 59 | Volume overload in pig 6, 24, 48, 96, 168 hours 2, 3 months | Initial increase during the acute (compensated) hypertrophic response (6 hour after surgery) and decrease with the progression of hypertrophy (from 168 hours up to 3 months) |
| van Veen et al. 60 | Transgenic hypertrophic mouse model of forced retinoic acid signaling 4–6 month old | Heterogeneous reduction of expression in left ventricle. The remodeling accompanied by a reduction in conduction velocity |
| Chu et al. 61 | Transgenic mice over expressing a constitutively active for of calcineurin | Cx43 protein markedly down‐regulated, dephosphorylated and redistributed from the intercalated discs to the lateral borders |
| Sarkar et al. 62 | Transgenic mice with cardiac‐specific overexpression of myotrophin 4, 8 month old | A reduction in Cx43 mRNA expression at 4 weeks of age, with an even further reduction at 9 months compared to nontransgenic |
| Darrow et al. 63 | Cultured neonatal rat ventricular myocyte, exposed to cAMP | Two‐fold increase in the total content of connexin43, an increase in the number of gap junctions after exposure of neonatal rat ventricular myocyte cultures to cAMP, significant increase in conduction velocity |
| Dodge et al. 64 | Cultured neonatal rat ventricular myocyte, exposed to angiotensin II | An increase in Cx43 content and in the number of gap junction profile in cultured neonatal rat ventricular myocytes exposed to angiotensin II |
| Zhuang et al. 65 | Cultured neonatal rat ventricular myocyte, strech model | Upregulation of intercellular junction proteins, paralleled by increase in propagation velocity. No changes in upstroke velocity of the action potential or cell size |
| Uzzaman et al. 66 | RVH, monocrotaline induced pulmonary hypertension | Thirty‐five percent decrease in gap junction area per intercalated disk after 4 weeks of right ventricular hypertrophy caused by monocrotaline‐induced pulmonary hypertension in the rat, concomitant with a 30% decrease in longitudinal conduction velocity |
| Yao et al. 67 | Cx43‐deficient mice | Clusters of cells expressing normal levels of Cx43 randomly interspersed among Cx43‐deficient myocytes |
| Gutstein et al. 68 | Cx43‐deficient mice | Heterogeneous Cx43 expression resulting in conduction defects |
| Wiegerinck et al. 45 | Pressure‐volume overload in rabbit | Reduction of connexin43 content in mid‐myocardium but unchanged in subepicardium, longitudinal and transversal subepicardial conduction velocities higher in animals with heart failure |