C1q/TNF-related protein 3 alleviates heart failure via attenuation of oxidative stress in myocardial infarction rats

Liu, Yu; Wu, Pinxia; Xu, Xiaohong; Shen, Tao; Wang, Xinxin; Liu, Yayuan; Chen, Yuan; Zhou, Limin; Ai, Liu

doi:10.1016/j.peptides.2023.170980

Cited by 3 publications

(1 citation statement)

References 23 publications

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“…Studies have found that CTRP3 overexpression can inhibit oxidative stress enhancement in myocardial infarction rat hearts. CTRP3 overexpression improved heart function and related myocardial fibrosis induced by myocardial infarction by inhibiting oxidative stress [ 27 ]. CTRP9 demonstrated significant protective effects against atherosclerosis, including enhancing plaque stability by activating AMPK, inhibiting levels of adhesion molecules in atherosclerotic plaques, and reducing MCP-1 and TNF-α secretion.…”

Section: Discussionmentioning

confidence: 99%

The clinical role of combined circulating complement C1q and AIP for CAD with LDL-C level below 1.8mmol/L

Hu,

Zhao,

Dong

et al. 2024

Lipids Health Dis

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Background In the past few years, circulating complement C1q involvement in atherosclerosis has garnered growing research interest in addition to the emerging recognition of the novel lipid marker named atherogenic index of plasma (AIP). Nevertheless, among patients experiencing low-density lipoprotein cholesterol (LDL-C) levels less than 1.8mmol/L, the interplay between C1q combined with the AIP for coronary artery disease (CAD) is ambiguous. Methods Patients were stratified into a non-CAD and CAD group according to their coronary angiography. The association between C1q in conjunction with the AIP and CAD was explored using restricted cubic spline analyses and logistic regression models. To assess how it predicted, a receiver operating characteristic analysis was undertaken. Results A total of 7270 patients comprised 1476 non-CAD patients and 5794 patients diagnosed with CAD were analyzed. A comparison of the two groups showed that the C1q levels were notably higher compared to the CAD group, while AIP exhibited an inverse trend. Across quartiles of C1q, the AIP demonstrated a decline with increasing C1q levels, and significant differences were observed between the groups. A correlation analysis underscored a notable negative correlation between the two variables. Univariate and multivariate logistic regression analyses revealed significant associations between CAD and the C1q quartile groups/AIP. Furthermore, compared with the Q4 group, a decrease in the C1q levels corresponded to an escalation in CAD risk, with the odds ratio rising from 1.661 to 2.314. Conclusions In conclusion, there appears to be a notable positive correlation between the combination of C1q with the AIP and CAD.

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Section: Discussionmentioning

confidence: 99%

The clinical role of combined circulating complement C1q and AIP for CAD with LDL-C level below 1.8mmol/L

Hu,

Zhao,

Dong

et al. 2024

Lipids Health Dis

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Upregulation of C1QC as a Mediator of Blood–Brain Barrier Damage in Type 2 Diabetes Mellitus

Huang,

Lin,

Chen

et al. 2024

Mol Neurobiol

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CTRP6‐mediated cardiac protection in heart failure via the AMPK/SIRT1/PGC‐1α signalling pathway

Fan,

Zhu,

et al. 2024

Experimental Physiology

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Heart failure (HF) remains a significant global health concern with limited effective treatments available. C1q/TNF‐related protein 6 (CTRP6) is a member of the CTRP family analogous to adiponectin and its role in HF pathogenesis remains unclear. Here, we investigated the impact of CTRP6 on HF progression. To mimic heart failure with reduced ejection fraction (HFrEF), we used isoproterenol injection in mice and administered adenovirus vectors expressing CTRP6 (Ad‐CTRP6) via tail vein injection. We assessed cardiac function through echocardiography and histology. CTRP6's effects on hypertrophy, fibrosis, apoptosis, oxidative stress and mitochondrial function were analysed. Downstream pathways (phosphorylated AMP‐activated protein kinase (p‐AMPK), sirtuin 1 (SIRT1) and peroxisome proliferator‐activated receptor γ coactivator 1‐α (PGC‐1α) were studied in heart tissues. In vitro, isoproterenol‐stimulated H9c2 cardiomyocytes were treated with CTRP6 to examine viability, apoptosis, F‐actin and signalling proteins. Compound C was used to assess AMPK involvement. CTRP6 expression was lower in the plasma of HF patients. In an isoproterenol‐induced HFrEF mouse model, adenovirus‐mediated overexpression of CTRP6 ameliorated cardiac dysfunction and reduced cardiomyocyte apoptosis, oxidative stress, inflammation and myocardial injury markers. Mechanistically, CTRP6 activation of the AMPK/SIRT1/PGC‐1α signalling pathway restored mitochondrial homeostasis, evidenced by reduced mitochondrial reactive oxygen species levels, increased ATP content, and enhanced mitochondrial complex I/III activities in cardiac tissues. In vitro studies using isoproterenol‐stimulated H9c2 cardiomyocytes corroborated these findings, demonstrating that CTRP6 upregulation attenuated hypertrophy, apoptosis, oxidative stress and mitochondrial dysfunction. Furthermore, these effects were partially reversed by the AMPK inhibitor Compound C, implicating the involvement of the AMPK pathway in CTRP6‐mediated cardioprotection. CTRP6 alleviates HF progression through the AMPK/SIRT1/PGC‐1α signalling pathway.

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C1q/TNF-related protein 3 alleviates heart failure via attenuation of oxidative stress in myocardial infarction rats

Cited by 3 publications

References 23 publications

The clinical role of combined circulating complement C1q and AIP for CAD with LDL-C level below 1.8mmol/L

The clinical role of combined circulating complement C1q and AIP for CAD with LDL-C level below 1.8mmol/L

Upregulation of C1QC as a Mediator of Blood–Brain Barrier Damage in Type 2 Diabetes Mellitus

CTRP6‐mediated cardiac protection in heart failure via the AMPK/SIRT1/PGC‐1α signalling pathway

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