Pathological findings of myocardium in a patient with cardiac conduction defect associated with an SCN5A mutation

Kawano, Hiroaki; Kawamura, Koichi; Kohno, Masaki; Ishijima, Mitsuaki; Fukae, Satoki; Ishikawa, Taisuke; Makita, Naomasa; Maemura, Koji

doi:10.1007/s00795-021-00283-9

Cited by 4 publications

(5 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Additionally, myocardial remodeling is the result of the combination of myocardial apoptosis, myocardial hypertrophy, and myocardial fibrosis [ 5 ]. There is accumulation of misfolded proteins and damaged organelles in hypertrophic cardiomyocytes [ 6 ], and autophagy can specifically remove misfolded proteins and damaged organelles, reducing their damage to cardiomyocytes [ 7 ]. The autophagy agonist, rapamycin, improved myocardial fibrosis and cardiac function in HF rats; when chloroquine was given to suppress autophagy, myocardial fibrosis in rats was aggravated and cardiac function deteriorated [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Inhibits Ventricular Remodeling in Heart Failure Rats by Activating Autophagy through AMPK/mTOR Pathway

2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

Objective. Heart failure (HF) is the end stage of heart disease caused by various factors which mainly involves ventricular remodeling (VR). In HF patients with reduced ejection fraction, dapagliflozin (DAPA) reduced the risk of worsening HF or cardiovascular death. Thus, we attempted to clarify the specific role of DAPA underlying HF progression. Methods. The HF rat model was established to mimic characteristics of HF in vivo. HE staining assessed histopathological changes in left ventricular myocardial tissue of rats in each group. ELISA measured plasma ANP and BNP levels of rats in each group. M-mode echocardiography detected cardiac function of rats in each group. TUNEL staining detected apoptosis of infarct margin cells in myocardial tissue of rats in each group. Western blot detected levels of apoptosis-related proteins, autophagy-related proteins, and AMPK/mTOR-related proteins in myocardial tissue of rats in each group. Immunohistochemical staining detected caspase-3 or LC3B level in myocardial tissue of rats in each group. The HF cellular model was established to mimic characteristics of HF in vitro. Flow cytometry detected H9C2 cell apoptosis under different conditions. Western blot detected levels of apoptosis-related proteins, autophagy-related proteins, and AMPK/mTOR-related proteins in H9C2 cells under different conditions. Immunofluorescence detected caspase-3 or LC3B level in H9C2 cells under different conditions. Results. DAPA attenuated left VR and improved cardiac function in HF rats. DAPA attenuated cardiomyocyte apoptosis in HF rats. DAPA facilitated cardiomyocyte autophagy in HF rats via the AMPK/mTOR pathway. DAPA repressed hypoxia-induced H9C2 cell apoptosis by facilitating autophagy. DAPA repressed hypoxia-induced H9C2 cell apoptosis via the AMPK/mTOR pathway. Conclusion. DAPA suppresses ventricular remodeling in HF through activating autophagy via AMPK/mTOR pathway, which provides a potential novel insight for seeking therapeutic plans of HF.

show abstract

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Inhibits Ventricular Remodeling in Heart Failure Rats by Activating Autophagy through AMPK/mTOR Pathway

2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

show abstract

“…10 Mais recentemente, há relato de acúmulo de lipofuscina nos cardiomiócitos hipertróficos de paciente de 16 anos de idade com defeito de condução cardíaca associada a mutação do gene da subunidade 5 alfa do canal de sódio voltagem-dependente (SCN5A). 11 Até onde sabemos há um único estudo focando a deposição de lipofuscina no miocárdio após o transplante cardíaco. 8 Nesse estudo os autores sugeriram que a detecção de lipofuscina em biópsias endomiocárdicas obtidas tardiamente (12 meses) após o transplante cardíaco poderia ser preditiva do desenvolvimento de DVE.…”

Section: Resultsunclassified

Section: Discussionunclassified

See 1 more Smart Citation

Distúrbio Cumulativo da Lipofuscina Miocárdica após Transplante Cardíaco de Longa Evolução: Estudo Baseado em Biópsias Endomiocárdicas

Benvenuti¹,

Marcondes‐Braga²,

Bacal³

2023

Arquivos Brasileiros De Cardiologia

View full text Add to dashboard Cite

show abstract

“…Among these, cardiomyocyte hypertrophy marks the initial phase of HF and, if left unchecked, accelerates cardiac function deterioration. Hypertrophic cardiomyocytes accumulate misfolded proteins and damaged organelles [19], which autophagy can effectively clear to mitigate their detrimental effects on cardiomyocytes. Myocardial fibro-Am J Transl Res 2024;16(5):1991-2000 1).…”

Section: Autophagy In Cardiomyocytes: Moderate Autophagy Delays Hf Pr...mentioning

confidence: 99%

Research progress of autophagy in heart failure

2024

Am J Transl Res

View full text Add to dashboard Cite

Heart failure poses a significant threat to global public health within the realm of cardiovascular diseases. Its pathological progression involves various alterations in cardiomyocytes, among which autophagy, a crucial intracellular degradation mechanism, plays a pivotal role. Autophagy facilitates the breakdown of damaged organelles and proteins, thereby maintaining cellular homeostasis. In the context of heart failure, autophagy coexists with apoptosis and necrosis, influencing myocardial hypertrophy and ventricular remodeling. However, its impact on heart failure manifests a dual nature: moderate autophagy aids in cardiac repair, whereas excessive autophagy may exacerbate ventricular remodeling and cell demise. This review delves into the fundamental biology of autophagy, elucidating its involvement in the pathological cascade of heart failure and its correlation with cardiac hypertrophy and ventricular remodeling. Furthermore, an analysis of the interplay between autophagy regulatory factors and heart failure sheds light on the potential therapeutic implications of autophagy in the prevention and management of heart failure. This exploration provides a theoretical foundation for novel treatment strategies in combating heart failure.

show abstract

Pathological findings of myocardium in a patient with cardiac conduction defect associated with an SCN5A mutation

Cited by 4 publications

References 15 publications

Dapagliflozin Inhibits Ventricular Remodeling in Heart Failure Rats by Activating Autophagy through AMPK/mTOR Pathway

Dapagliflozin Inhibits Ventricular Remodeling in Heart Failure Rats by Activating Autophagy through AMPK/mTOR Pathway

Distúrbio Cumulativo da Lipofuscina Miocárdica após Transplante Cardíaco de Longa Evolução: Estudo Baseado em Biópsias Endomiocárdicas

Research progress of autophagy in heart failure

Contact Info

Product

Resources

About