You described something, but completely failed at telling us the significance or what needs to be done. I'd fire your mentors and senior researchers also for incompetence!
Association between circulating plasma CTRP3 levels and acute ischemic stroke: a systematic review and meta-analysis
- 1Department of Emergency Medicine, West China Hospital of Sichuan University, Sichuan University, Chengdu, China
- 2Laboratory of Emergency Medicine, Disaster Medical Center, West China Hospital of Sichuan University, Chengdu, China
- 3West China School of Medicine, Sichuan University, Chengdu, China
Background: C1q tumor necrosis factor (TNF)-related protein 3 (CTRP3) is a novel adipokine that has been shown to exert neuroprotective effects in acute cerebral infarction. However, conflicting results have emerged regarding the circulating levels of CTRP3 between patients with acute ischemic stroke and healthy individuals. This meta-analysis aims to investigate the association between circulating CTRP3 levels and acute ischemic stroke.
Objective: The objective of this meta-analysis is to re-evaluate the relationship between circulating CTRP3 levels and acute ischemic stroke.
Methods: We conducted a comprehensive search across PubMed, Web of Science, Embase, Cochrane Library, CNKI, VIP, Wanfang Data, and CBM to identify relevant studies up to February 2025 and 110 articles were found. After screening the titles, abstracts, and full texts, a total of 14 articles were ultimately included in this meta-analysis. Due to high heterogeneity, we conducted subgroup analyses stratified by patient characteristics, clinical and biochemical parameters, carotid intima-media thickness, IL-6 levels, CTRP9 levels, smoking, hypertension, and diabetes. Publication bias was evaluated using Egger’s regression test, Begg’s correlation analysis, and funnel plot visualizations.
Results: The results indicated that patients with acute ischemic stroke exhibited significantly lower circulating levels of CTRP3 compared with control group (Z = 6.04, P < 0.00001). Subgroup analysis revealed that the observed heterogeneity could be attributed to patient age and body mass index (BMI). The year of publication, clinical biochemical parameters, carotid intima-media thickness, IL-6, CTRP9, smoking, hypertension, and diabetes categorization were not sources of heterogeneity.
Conclusion: The meta-analysis confirmed that circulating levels of CTRP3 were significantly lower(Meaning what? Not answering that is pure incompetence!) in patients with acute ischemic stroke compared with control group. This association may be modulated by patient age and BMI.
Introduction
Acute ischemic stroke (AIS) is a leading cause of disability and death globally, imposing a staggering burden at both individual and societal levels (Katan and Luft, 2018). The complex physiological mechanisms of the brain have led to the current lack of stroke-specific biomarkers (Salaudeen et al., 2024). Thus, it is important to investigate the relevant risk factors following acute ischemic stroke for early detection and prevention in clinical practice.
The novel adipokine complement C1q/tumor necrosis factor-related protein 3 (CTRP3) is associated with inflammation, atherosclerosis, and the regulation of various physiological and pathological processes (Li Y. et al., 2017). CTRP3 is a highly hydrophilic secreted protein, with an N-terminal hydrophobic signal peptide, and no transmembrane domains. CTRP3 was first discovered in 2001 was originally named CORS26 (Collagenous repeat-containing sequence 26 kDa protein) (Maeda et al., 2001). CTRP3 has also been referred to as cartducin and cartonectin, names derived from its observed expression in embryonic cartilage tissue (Maeda et al., 2006). Two splice variants of CTRP3 have been identified to date. The longer isoform, referred to as CTRP3B, results from the retention of intron 1 and includes an additional 73 amino acids at the N-terminus, along with a conserved N-linked glycosylation site not present in the shorter isoform, CTRP3A. Although the specific physiological roles of these variants remain to be elucidated, both isoforms are secreted and detectable in human serum (Peterson et al., 2010). Although CTRP3 has not been definitively confirmed to have a specific receptor, some studies suggest that its functions may be mediated through AdipoR2 (Adiponectin receptor 2) (Murayama et al., 2021). Prior studies have shown AdipoR2 expression in neurons and glial cells in the ischemic penumbra (Clain et al., 2022). In addition, previous studies have demonstrated that CTRP3 can activate the PI3K/Akt, MAPK/ERK, and AMPK signaling pathways, which are typically mediated by membrane receptors, suggesting the existence of an as-yet unidentified binding mechanism between CTRP3 and membrane receptors (Guo et al., 2020).
In recent years, an increasing number of studies have found that CTRP3 is associated with various inflammatory diseases. For example, serum CTRP3 levels are significantly elevated in patients with Hashimoto’s disease compared to controls (Al-Abboody et al., 2025), while circulating CTRP3 levels are markedly reduced in male patients with coronary syndrome (Schmid et al., 2024). Meanwhile, CTRP3 levels are significantly downregulated in asthmatic mice (Lin and Yi, 2023). In addition, in mouse models of rheumatoid arthritis, CTRP3 is markedly increased in two different models (Murayama et al., 2014). In a mouse model of autoimmune encephalomyelitis, CTRP3 inhibits Th17 cell differentiation and exhibits anti-inflammatory effects (Murayama et al., 2021). These evidences enhance the clinical relevance of CTRP3 and support its role as a systemic inflammatory marker. Mounting evidence indicates that inflammatory processes are critically involved in the onset and progression of acute ischemic stroke (Ahmad et al., 2014). Alterations of CTRP3 levels may be associated with the onset of acute ischemic stroke (Sun et al., 2021). Currently, few studies have reported on the changes in serum CTRP3 levels in patients with acute ischemic stroke, with the majority of research focusing on Chinese studies. The predictive value of CTRP3 for acute ischemic stroke remains unclear. In addition, conflicting results have emerged regarding the association between circulating CTRP3 levels and acute ischemic stroke. Therefore, our study aims to explore the relationship between circulating CTRP3 levels and acute ischemic stroke.
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Ziyi Zhu3
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