# Role of apelin as a biomarker in functional recovery and post-stroke-associated sarcopenia: insights from rehabilitation therapy

**Authors:** Da-Jung Lee, Dong Kyu Choi, Joong-Gook Kim, Wanil Kim, Hwan-Kwon Do

PMC · DOI: 10.7717/peerj.20820 · PeerJ · 2026-03-06

## TL;DR

This study shows that rehabilitation in stroke patients increases apelin levels, which are linked to better muscle health and recovery.

## Contribution

The study identifies apelin as a potential biomarker for monitoring muscle recovery and rehabilitation outcomes in stroke patients.

## Key findings

- Apelin levels increased significantly after rehabilitation in stroke patients.
- Higher apelin levels correlated with improved skeletal muscle index and functional outcomes.
- Rehabilitation also led to reduced fatigue and better quality of life in stroke survivors.

## Abstract

Skeletal muscles play critical roles in mobility, respiratory function, and metabolic regulation by releasing myokines. Age-related sarcopenia, characterized by the loss of muscle mass and function, exacerbates health outcomes, including disability and mortality. Stroke survivors are particularly vulnerable to muscle wasting, known as stroke-related sarcopenia, which affects their recovery and quality of life. This study aimed to investigate the effects of rehabilitation on apelin expression, clinical outcomes, and psychosocial well-being in stroke survivors.

This single-center observational study enrolled 23 patients with stroke who underwent rehabilitation. Outcome measures included apelin concentration using enzyme-linked immunosorbent assay, cytokine profiling, skeletal muscle index (SMI), phase angle, grip strength, balance, functional scores (Modified Barthel Index, Berg Balance Scale), and psychosocial measures (SF-12, Fatigue Severity Scale). Data were collected at baseline and discharge after 4–6 weeks of rehabilitation.

Apelin levels increased significantly after rehabilitation (46.81–59.23 ng/mL, p < 0.001) and correlated with improved SMI (6.67–7.11 kg/m2, p = 0.0035) and functional outcomes (p < 0.001). Significant changes in the cytokine profiles highlighted exercise-induced anti-inflammatory responses. Psychosocial assessments revealed reduced fatigue and improved quality of life (p < 0.001).

Stroke patient rehabilitation enhanced apelin expression, skeletal muscle mass, and functional recovery. Therefore, apelin may serve as a biomarker to monitor muscle health and rehabilitation outcomes.

## Linked entities

- **Diseases:** stroke (MONDO:0005098)

## Full-text entities

- **Genes:** APLNR (apelin receptor) [NCBI Gene 187] {aka AGTRL1, APJ, APJR, HG11}, PCS [NCBI Gene 8075], APLN (apelin) [NCBI Gene 8862] {aka APEL, XNPEP2}, PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891] {aka LEM6, PGC-1(alpha), PGC-1alpha, PGC-1v, PGC1, PGC1A}, BBS2 (Bardet-Biedl syndrome 2) [NCBI Gene 583] {aka BBS, RP74}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, FUT4 (fucosyltransferase 4) [NCBI Gene 2526] {aka CD15, ELFT, FCT3A, FUC-TIV, FUTIV, LeX}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, CCL17 (C-C motif chemokine ligand 17) [NCBI Gene 6361] {aka A-152E5.3, ABCD-2, SCYA17, TARC}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562] {aka AMPK, AMPK alpha 1, AMPKa1}, CCR4 (C-C motif chemokine receptor 4) [NCBI Gene 1233] {aka CC-CKR-4, CD194, CKR4, CMKBR4, ChemR13, HGCN:14099}, GPRC5D (G protein-coupled receptor class C group 5 member D) [NCBI Gene 55507]
- **Diseases:** decline in skeletal muscle mass (MESH:C536030), SMI (MESH:D005207), cognitive frailty (MESH:D000073496), difficulties (MESH:D051346), neurological deficits (MESH:D009461), Fatigue (MESH:D005221), paralysis (MESH:D010243), Post-stroke (MESH:D020521), hemiplegic symptoms (MESH:D020233), hemorrhagic (MESH:D006470), obese (MESH:D009765), hemorrhagic stroke (MESH:D000083302), functional dependency (MESH:D019966), cancer (MESH:D009369), ischemic (MESH:D002545), weakness (MESH:D018908), NIHSS (MESH:C538175), fractures (MESH:D050723), physical disability (MESH:D059445), Sarcopenia (MESH:D055948), inflammation (MESH:D007249), muscle wasting (MESH:D009133), disability (MESH:D009069), cognitive and (MESH:D003072), sepsis (MESH:D018805), FSS (MESH:D045169), loss of muscle mass and function (MESH:D009135), depression (MESH:D003866), renal impairment (MESH:D007674), vascular dysfunction (MESH:D002561), insulin resistance (MESH:D007333), age-related muscle decline (MESH:D010024), infection (MESH:D007239), ischemic stroke (MESH:D002544), hypertrophy (MESH:D006984), coronavirus disease 2019 infection (MESH:D000086382), end-stage renal disease (MESH:D007676), malnutrition (MESH:D044342), hip fracture (MESH:D006620), mobility impairments (MESH:D014086), vertebral compression fracture (MESH:D050815), MI (MESH:C566784)
- **Chemicals:** nitric oxide (MESH:D009569), EDTA (MESH:D004492), prostaglandin (MESH:D011453)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

59 references — full list in the complete paper: https://tomesphere.com/paper/PMC12970307/full.md

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Source: https://tomesphere.com/paper/PMC12970307