TRPC3 deficiency attenuates high salt-induced cardiac hypertrophy by alleviating cardiac mitochondrial dysfunction

Ma, Tianyi; Lin, Shaoyang; Wang, Bin; Wang, Qianran; Xia, Weijie; Zhang, Hexuan; Cui, Yuanting; He, Chengkang; Wu, Hao; Sun, Fang; Zhao, Zhigang; Gao, Peng; Zhu, Zhiming; Liu, Daoyan

doi:10.1016/j.bbrc.2019.09.018

Cited by 28 publications

(21 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ma et al reported that high salt treatment aggravated ROS production in mitochondria by transient receptor potential channel canonical 3, and as a result, expression of plasma BNP levels was increased. [ 21 ] Unfortunately, we could not examine the causal relationships between plasma BNP levels and salt intake levels because this study was performed on participants attending their regular annual health check-ups. However, it is possible that inflammation and ROS causes elevated plasma BNP levels through high salt levels.…”

Section: Discussionmentioning

confidence: 99%

Salt intake causes B-type natriuretic peptide elevation independently of blood pressure elevation in the general population without hypertension and heart disease

et al. 2021

View full text Add to dashboard Cite

Excessive salt intake causes hypertension and cardiovascular diseases (CVDs). B-type natriuretic peptide (BNP) is synthesized and released from the ventricle, and is a surrogate marker reflecting various CVDs. Moreover, when a slight BNP elevation is shown, it leads to a poor prognosis in the general population. However, the relationship between salt intake and BNP levels in the general population remains unclear, especially in those without hypertension and heart diseases. In this study, we recruited 1404 participants without hypertension and electrocardiogram abnormalities, who received regular annual health check-ups in Japan. Plasma BNP levels were measured, and daily salt intake levels were evaluated using urinary samples. In addition, some clinical parameters were obtained, and the data were cross-sectionally analyzed. The median of plasma BNP levels was 10.50 pg/mL, and daily salt intake was 8.50 ± 1.85 g. When dividing participants into quartiles according to daily salt intake, those with the highest daily salt intake revealed the highest plasma BNP levels. Plasma BNP levels were significantly and positively associated with daily salt intake. Moreover, multiple linear regression analyses revealed that plasma BNP levels showed a significant positive association with daily salt intake levels after adjustments. Plasma BNP levels were significantly and positively associated with daily salt intake after adjustment in the general population. Plasma BNP levels may be a surrogate marker reflecting salt-induced heart diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Salt intake causes B-type natriuretic peptide elevation independently of blood pressure elevation in the general population without hypertension and heart disease

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Besides, a HSD could inhibit potassium channels ( Oloyo et al, 2013 ). In addition, recent evidence showed that several transient receptor potential channels (TRP), including TRPV1 and TRPC3, are involved in high-salt intake–induced cardiac hypertrophy by mediating mitochondrial function via regulating mitochondrial calcium uptake ( Lang et al, 2015 ; Ma et al, 2019 ). Thus, high-salt intake–mediated activation or inactivation of important ion channels in myocytes or vascular muscle cells could also be therapeutically useful for high-salt intake–induced hypertension and cardiac dysfunction, which remains to be further investigated in the future.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

Mao

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

The present study aimed to explore whether high-salt diet (HSD) could cause cardiac damage independent of blood pressure, and whether nitric oxide (NO) could alleviate high-salt–induced cardiomyocyte apoptosis and autophagy in rats. The rats received 8% HSD in vivo. H9C2 cells or primary neonatal rat cardiomyocytes (NRCM) were treated with sodium chloride (NaCl) in vitro. The levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1 and autophagy related 7 (ATG7) were increased in the heart of HSD rats with hypertension (HTN), and in hypertension-prone (HP) and hypertension-resistant (HR) rats. Middle and high doses (50 and 100 mM) of NaCl increased the level of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in H9C2 cells and NRCM. The endothelial NO synthase (eNOS) level was increased, but p-eNOS level was reduced in the heart of HSD rats and H9C2 cells treated with 100 mM NaCl. The level of NO was reduced in the serum and heart of HSD rats. NO donor sodium nitroprusside (SNP) reversed the increases of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2 induced by NaCl (100 mM) in H9C2 cells and NRCM. SNP treatment attenuated the increases of cleaved-caspase 3/caspase 3, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in the heart, but had no effect on the blood pressure of HSD rats with HR. These results demonstrated that HSD enhanced cardiac damage independently of blood pressure. Exogenous NO supplementarity could alleviate the high salt–induced apoptosis and autophagy in cardiomyocytes.

show abstract

“…Transient receptor potential channel, canonical 3(TRPC3), residing in mitochondria, also exerted regulatory roles in high salt-induced cardiac hypertrophy by mediating mitochondrial function. TRPC3 ablation antagonized cardiac hypertrophy induced by high salt intake, which was achieved by restoring the synthesis of ATP and the activity of complex I and II enzyme in mitochondria ( 39 ).…”

Section: Mechanisms Linking Mitochondria and Pathological Cardiac Hypertrophymentioning

confidence: 99%

Mitochondria in Pathological Cardiac Hypertrophy Research and Therapy

Yang

Liu

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Cardiac hypertrophy, a stereotypic cardiac response to increased workload, ultimately progresses to severe contractile dysfunction and uncompensated heart failure without appropriate intervention. Sustained cardiac overload inevitably results in high energy consumption, thus breaking the balance between mitochondrial energy supply and cardiac energy demand. In recent years, accumulating evidence has indicated that mitochondrial dysfunction is implicated in pathological cardiac hypertrophy. The significant alterations in mitochondrial energetics and mitochondrial proteome composition, as well as the altered expression of transcripts that have an impact on mitochondrial structure and function, may contribute to the initiation and progression of cardiac hypertrophy. This article presents a summary review of the morphological and functional changes of mitochondria during the hypertrophic response, followed by an overview of the latest research progress on the significant modulatory roles of mitochondria in cardiac hypertrophy. Our article is also to summarize the strategies of mitochondria-targeting as therapeutic targets to treat cardiac hypertrophy.

show abstract

TRPC3 deficiency attenuates high salt-induced cardiac hypertrophy by alleviating cardiac mitochondrial dysfunction

Cited by 28 publications

References 37 publications

Salt intake causes B-type natriuretic peptide elevation independently of blood pressure elevation in the general population without hypertension and heart disease

Salt intake causes B-type natriuretic peptide elevation independently of blood pressure elevation in the general population without hypertension and heart disease

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

Mitochondria in Pathological Cardiac Hypertrophy Research and Therapy

Contact Info

Product

Resources

About