APLN ELISA kit
- Known as:
- APLN Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APLN-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APLN ELISA kit
Related genes to: APLN ELISA kit
- Gene:
- APLN NIH gene
- Name:
- apelin
- Previous symbol:
- -
- Synonyms:
- apelin, XNPEP2
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-01
- Date modifiied:
- 2016-10-05
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- Multiple sclerosis (MS) is an autoimmune disorder with a complex and multifactorial etiology. Increasing evidence suggests that peptide hormones may significantly influence the pathogenesis of MS by affecting inflammatory processes and metabolic dysregulation. The aim of the study was to evaluate the levels of apelin and ghrelin, which are two peptide hormones, in patients with relapsing-remitting MS (RRMS) receiving natalizumab and fingolimod compared to healthy controls. - Source: PubMed
Publication date: 2026/04/28
Adamczyk BożenaMorawiec NataliaRakoca MichałSowa AgataSawa KsawierAdamczyk-Sowa Monika - Diabetic foot ulcers (DFUs) represent a severe chronic complication of diabetes and are characterized by persistent impairment of wound healing, accompanied by defective angiogenesis, chronic inflammation, and dysregulated extracellular matrix remodeling. Although impaired angiogenesis is widely recognized as a key pathological feature of DFUs, its associated molecular alterations have not been systematically characterized at the transcriptomic and cellular levels. - Source: PubMed
Publication date: 2026/05/13
Hu XiangjunDong DegangWang YunfeiCai HongYin HongweiYan Zhangren - Anthracycline-induced cardiotoxicity remains a major clinical challenge, often progressing to heart failure years after therapy. Conventional cardioprotective agents, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and beta-blockers, are widely used to preserve cardiac function; however, their effectiveness is limited by their inability to comprehensively address the complex, multifactorial pathophysiology of anthracycline-induced cardiotoxicity. This underscores the critical need for more effective and mechanism-based cardioprotective strategies that directly target the underlying molecular mechanisms, particularly oxidative stress and mitochondrial dysfunction. In recent years, the apelin-APJ signalling axis has attracted increasing attention as a potential therapeutic target in cardiovascular diseases owing to its multifaceted biological actions, including positive inotropy, vasodilation, anti-inflammatory, anti-fibrotic, anti-apoptotic, antioxidant, and pro-angiogenic effects. These pleiotropic actions are primarily mediated through the activation of key signalling pathways such as phosphoinositide 3-kinase/protein kinase B, extracellular signal-regulated kinases 1/2, and AMP-activated protein kinase. Given that these signalling cascades are disrupted during anthracycline-induced cardiotoxicity, pharmacological activation of the apelin-APJ axis may represent a promising avenue to mitigate anthracycline-associated cardiac injury with greater efficacy than conventional therapies. While native apelin isoforms (apelin-12, -13, -17, and [Pyr¹]apelin-13) are limited by their short half-lives, chemically modified analogues such as LIT01-196 and apelin-17(A2) exhibit enhanced stability and efficacy, with demonstrated cardioprotective effects in preclinical cardiovascular models and patients with chronic heart failure. However, their therapeutic potential in anthracycline-induced cardiotoxicity remains largely unexplored. This review highlights its promise as a novel cardioprotective strategy for mitigating anthracycline-induced cardiotoxicity. - Source: PubMed
Publication date: 2026/04/17
Desai Varsha G - Elucidating the mechanisms underlying vascular injury and repair may guide development of therapies against vascular cognitive impairment and dementia (VD). We employed single-cell RNA sequencing to map cell populations and explore vascular responses in mouse brains collected 42 days after asymmetric common carotid artery stenosis (ACAS)-induced chronic cerebral hypoperfusion. A unique tip cell type was identified among endothelial cell (EC) clusters and validated by immunostaining. Gene Ontology analyses suggested tip cell enrichment in angiogenesis and the involvement of Apln/Aplnr signaling. Immunoblotting confirmed an increase in apelin (Apln) protein after ACAS. In EC cultures, [Pyr1]-Apelin-13 (Apln13), a selective endogenous apelin receptor agonist, enhanced EC proliferation, migration, and tube formation. Treatment with Apln13 also improved angiogenesis, white matter integrity, and cognitive functions in ACAS mice. Cell-cell interaction analyses highlighted astrocyte-tip cell crosstalk via Vegfa-Vegfr interactions. - Source: PubMed
Publication date: 2026/03/11
Shan JiajingShi RuyuJiang LiyuanDufort ConnorMiao WanyingMai Ting-WeiLyu JunxuanBarreiro JulietaChen KongLeak Rehana KChen JunHu Xiaoming - Emerging evidence suggests that apelinergic peptides and components of the renin-angiotensin system (RAS) are key regulators of cardiovascular homeostasis and fluid balance, both disrupted in chronic kidney disease (CKD). This study aimed to assess serum levels of apelin, elabela, and angiotensinogen across the CKD spectrum and evaluate their acute modulation during a single hemodialysis (HD) session. Serum samples from healthy controls ( = 21), non-dialysis CKD patients ( = 21), and HD patients ( = 44) were analyzed using high-sensitivity immunoassays. In HD patients, matched samples were collected before and after dialysis. - Source: PubMed
Publication date: 2026/03/26
Serwin Natalia MariaCecerska-Heryć ElżbietaGrygorcewicz BartłomiejCejko MateuszJerzyk AdriannaĆwikła KacperSpajzer EmiliaManelska AleksandraWoźniak PaulinaGomółka AleksandraCader-Ptak AleksandraBąk KatarzynaLisak MarcinOpara-Bajerowicz MartynaWojciuk BartoszSuwała MariuszSerwin KarolWiśniewska MagdaDołęgowska Barbara