Intermittent exercise alleviates MI-induced renal injury in mice via IGF-1.

Zhu W, Bo W, Ma Y

Frontiers in physiology19 Dec 2025Cited by 1 (Europe PMC)

PMID41488924PMCIDPMC12757210DOI10.3389/fphys.2025.1733425PepBankPUB-41488924

Summary

Myocardial infarction (MI) often induces acute kidney injury (AKI) via systemic hypoperfusion and oxidative stress, yet the protective mechanisms of exercise remain unclear. This study investigated whether intermittent exercise alleviates MI-induced AKI through the insulin-like growth factor-1 (IGF-1)/PI3K/AKT signaling pathway. An AKI model was established in mice via coronary artery ligation, followed by moderate-intensity intermittent treadmill training for 4 weeks. Echocardiography, serum biochemical markers, renal histology, RT-qPCR, and Western blotting were used to assess cardiac and renal function, inflammatory cytokines, oxidative stress, apoptosis, and IGF-1/PI3K/AKT signaling. In vitro, H₂O₂-treated NRK renal cells were used to mimic oxidative damage. Recombinant human IGF-1 (rhIGF-1), AMPK agonist AICAR, IGF-1 receptor inhibitor NVP-AEW541, and PI3K inhibitor LY294002 were applied to explore the pathway's involvement in exercise-induced renoprotection. MI led to impaired cardiac function, renal structural injury, elevated BUN and MDA levels, increased expression of IL-6, TNF-α, Bax, and Cleaved Caspase-3, and decreased SOD activity. Intermittent exercise improved cardiac output, attenuated renal injury, enhanced antioxidant capacity, and upregulated IGF-1 expression and its downstream PI3K/AKT signaling. In vitro, rhIGF-1 and AICAR mimicked the protective effects of exercise, while IGF-1R or PI3K inhibitors partially abolished these effects. These findings suggest that intermittent exercise ameliorates MI-induced AKI by activating the IGF-1/PI3K/AKT pathway, thereby exerting anti-inflammatory, antioxidant, and anti-apoptotic effects. This study highlights the role of exercise-induced IGF-1 in heart-kidney axis protection and provides a mechanistic basis for therapeutic interventions targeting MI-related renal complications.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Efficacy outcome
In oxidatively damaged NRK renal cells, AICAR mimicked the protective effects of exercise, without separate cellular endpoint results being specified.
In plain wordsIn cells with oxidative damage, AICAR mimicked exercise's protective effects, but the abstract does not specify individual cellular results.
Peptide
AICAR (acadesine)
Outcome
Direction not reportedProtective effects in renal cells
Study
n: not reported in source
H2O2-treated NRK renal cells
Outcome group
Kidney function · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
In vitro, rhIGF-1 and AICAR mimicked the protective effects of exercise, while IGF-1R or PI3K inhibitors partially abolished these effects.
2 context sentences(design, population, supporting numbers)
Summary · context
In vitro, H₂O₂-treated NRK renal cells were used to mimic oxidative damage.
Summary · context
Recombinant human IGF-1 (rhIGF-1), AMPK agonist AICAR, IGF-1 receptor inhibitor NVP-AEW541, and PI3K inhibitor LY294002 were applied to explore the pathway's involvement in exercise-induced renoprotection.
Show in the study text Report a problemFND-4148892401

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Version history

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Version 2Current
21 Oct 2026, 15:58 UTC
Study results updated
Version 1
21 Oct 2026, 12:50 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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