Objective To systematically review the relationship between circulating C1q/TNF-related protein 9 (CTRP9) levels and ischemic stroke (IS). Methods The PubMed, Web of Science, Embase, Cochrane Library, CNKI, WanFang Data, VIP databases were electronically searched to collect studies related to the objectives from database inception to February 2025. Two reviewers independently screened the literature, extracted data, and assessed the risk of bias of the included studies. Meta-analysis was then performed using RevMan 5.3 software and Stata 15.1 software. Results A total of 13 studies were included, and the meta-analysis results showed that the serum CTRP9 level in IS patients was significantly lower than that in non IS group (P<0.001). The results of subgroup analysis suggested that TG, LDL, and CTRP3 levels may be the source of heterogeneity, while the basic characteristics of the studies (publication year, average age of patients, BMI, research area, and unit of CTRP9) and the degree of carotid atherosclerosis were not the influencing factors of heterogeneity. Conclusion The meta-analysis confirms that serum CTRP9 level in IS patients is significantly lower than that in patients without IS. The association may be modified by TG, LDL, and CTRP3 levels. Due to the limited quantity and quality of the included studies, more high-quality studies are needed to verify the above conclusion.
Effective neuroprotective strategies are still lacking for cerebral ischemia-reperfusion injury secondary to ischemic stroke and cardiac arrest-cardiopulmonary resuscitation. Growing evidence suggests that adiponectin (APN) and its receptors exert pivotal protective effects in these pathological processes. This article summarizes the underlying mechanisms and translational potential of the APN signaling pathway. Exogenous interventions, including recombinant APN, APN peptides, and gene transfection, exert neuroprotective effects through multiple mechanisms such as anti-inflammatory and antioxidant actions, attenuation of excitotoxicity, and inhibition of apoptosis. Endogenous regulatory strategies, such as exercise preconditioning and pharmacological interventions, can upregulate APN and its receptor expression to mitigate injury. In addition, members of the APN homologous CTRP family exhibit synergistic neuroprotective potential. Integrating evidence from basic and clinical studies, targeting the APN pathway provides a promising therapeutic strategy for cerebral ischemia–reperfusion injury.
