BACKGROUNDRecent studies suggest that the loss of lysosomal function is associated with acute kidney injury (AKI), potentially leading to impaired autophagy. Apelin has been known to regulate autophagy processes in cardiovascular and pulmonary diseases. We sought to explore its potential contribution in lysosomal function and autophagy modulation during AKI.METHODSApelin-13 (30 μg/kg) or a vehicle control was administered to mice intraperitoneally 24 h prior to and at 0 h, 24 h, and 48 h following renal ischemia-reperfusion (I/R) injury or a sham procedure. Kidney and serum samples were collected for analysis 24 or 72 h postoperatively.RESULTSOur findings indicate that apelin-13 significantly mitigated renal damage and inhibited apoptosis post-AKI. Flow cytometry analysis revealed that apelin-13 treatment modulates the macrophages polarization within the kidney from M1 to M2 phenotype. Additionally, apelin-13 was found to reduce the expression of the (pro)renin receptor, restore lysosomal membrane permeability, augment lysosomal biogenesis, and enhance autophagic flux in the kidney following AKI.CONCLUSIONSOur study elucidates novel mechanisms underlying the protective effects of apelin in AKI through modulating lysosomal function and autophagy.

01 Aug 2025·Tissue and Cell

Apelin-13/APJ promotes neural stem cells to repair ischemic stroke

Article

Author: Meng, Cuicui ; Zhou, Changqing ; Wu, Haidong ; Wang, Tong ; Long, Huibao ; Huang, Zijie ; Xie, Yibei ; Zhong, Yinsheng ; Guo, Yajie ; Yuan, Sijun ; Pei, Liying ; Yang, Shujun ; Chen, Xuxiang ; Li, Shuangmei

Neural stem cell therapy is considered as a promising new therapy for ischemic stroke. However, the therapeutic efficacy of neural stem cells (NSCs) is hampered by the effects of cerebral ischemia and hypoxia, resulting in suboptimal performance. Drug stimulation can further improve the efficacy of NSCs in ischemic stroke, among which the small molecule peptide Apelin-13 could have the potential. In this study, we simulated the ischemic anoxic microenvironment by oxygen-glucose deprivation (OGD) to observe the improvement of Apelin-13 on NSCs treatment-related functions. Six hours of OGD treatment suppressed the cell viability of NSCs, while 100 nM Apelin-13 mitigated this suppression. Additionally, OGD treatment reduced the migration capability of NSCs, but Apelin-13 enhanced this ability under OGD conditions. OGD also increased the rate of apoptotic NSCs and decreased the ratio of Bcl-2 to Bax. In the OGD environment, BDNF expression was elevated, and Apelin-13 further increased this level. APJ is the endogenous receptor of Apelin-13. We knocked down the expression of APJ and observed that the effect of Apelin-13 on NSCs was abolished in the OGD environment compared with the negative control group with knockdown, and the upregulation of the expression of brain derived neurotrophic factor (BDNF) was also lost. Our study found that Apelin-13 enhances the cell viability of NSCs, fosters cell migration, diminishes apoptosis, and augments the expression of BDNF under conditions of OGD through the APJ receptor. The stimulation of the Apelin-13/APJ system may play a beneficial role in activating endogenous NSCs for the purpose of treating ischemic stroke. This positive effect may be mediated by the downstream effector protein, BDNF.

01 Mar 2025·Journal of Controlled Release

ROS-differentiated release of Apelin-13 from hydrogel comprehensively treats myocardial ischemia-reperfusion injury

Article

Author: Zhen, Penghao ; Yu, Fuchao ; Liang, Gaolin ; Tong, Jiayi ; Liu, Xiaoyang ; Wei, Qin ; Xu, Xuan ; Sun, Xianbao ; Jiang, Qiaochu

Treatment of myocardial ischemia-reperfusion (MI/R) injury still faces the lack of clinically approved drugs. Apelin-13 is a highly promising drug candidate of MI/R injury, but hampered by its extremely short half-life in plasma. This calls for efficient and smart delivering system for Apelin-13 delivery, but has not been reported. Herein, a reactive oxygen species (ROS)-responsive hydrogelator YFF-TK-FFY is designed, which co-assembles with Apelin-13 to form the peptide hydrogel Apelin-13@Gel TK. This hydrogel responds to ROS at varying levels in the surrounding environment of MI/R and releases Apelin-13 at different rates. In an MI/R injury mouse model, Apelin-13@Gel TK rapidly releases Apelin-13 in response to the high ROS in the core area of MI/R injury, efficiently reducing cardiomyocyte apoptosis within three days. In the ROS-low border zone, Apelin-13@Gel TK provides a slow and sustained release of Apelin-13, promoting angiogenesis and lymphatic remodeling, and facilitating the resolution of inflammation in the later repair stage after MI/R injury. By offering a spatiotemporally controlled drug release in response to ROS gradients in the MI/R microenvironment, this smart hydrogel presents a promising therapeutic strategy for effective treatment of MI/R injury.

100 Deals associated with Apelin-13

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Indication	Highest Phase	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	Phase 1	-	Le Centre Hospitalier Universitaire de Toulouse	-

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


Pubmed \| J Mol Cell Cardiol	Not Applicable	-	-	Apelin-13	(jslmthchxv) = Apelin also increased I(Na) "window" current by up to 600% logrpolzff (tzdftsxyty )	-	01 Apr 2010
				Apelin-17

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