Sustained activation of AMPK ameliorates age-associated vascular endothelial dysfunction via a nitric oxide-independent mechanism.

Lesniewski LA, Zigler MC, Durrant JR, Donato AJ, Seals DR

Mechanisms of ageing and development28 Mar 2012Cited by 50 (Europe PMC)

PMID22484146PMCIDPMC3359767DOI10.1016/j.mad.2012.03.011PepBankPUB-22484146

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study3

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

01AnimalAnimal study (in vivo)Mechanism
In old mice, AICAR increased arterial AMPK.
In plain wordsIn old mice, AICAR increased arterial AMPK.
Peptide
AICAR (acadesine)
Outcome
IncreaseArterial AMPK
Study
mousen: not reported in source
old B6D2F1 mice
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated · 2 weeksAs given in this study (mouse).
Source sentences
Summary
Pharmacological activation of AMPK by aminoimidazole carboxamide ribonucleotide (AICAR) for 2 weeks increased arterial AMPK and reversed this superoxide-induced impairment of EDD.
1 context sentence(design, population, supporting numbers)
Summary · context
Old (28-30 months) B6D2F1 mice had reduced arterial AMPK expression and superoxide-mediated suppression of EDD vs. young (3-6 months) controls.
Report a problemFND-2248414601
02AnimalAnimal study (in vivo)Efficacy outcome
In old mice, AICAR reversed superoxide-induced impairment of endothelium-dependent dilation.
In plain wordsIn old mice, AICAR reversed the impairment of artery dilation associated with superoxide.
Peptide
AICAR (acadesine)
Outcome
IncreaseEndothelium-dependent dilation
Study
mousen: not reported in source
old B6D2F1 mice
Outcome group
Vascular function · Cardiovascular
Studied dose
Dose not stated · 2 weeksAs given in this study (mouse).
Source sentences
Summary
Pharmacological activation of AMPK by aminoimidazole carboxamide ribonucleotide (AICAR) for 2 weeks increased arterial AMPK and reversed this superoxide-induced impairment of EDD.
1 context sentence(design, population, supporting numbers)
Summary · context
Old (28-30 months) B6D2F1 mice had reduced arterial AMPK expression and superoxide-mediated suppression of EDD vs. young (3-6 months) controls.
Report a problemFND-2248414602
03AnimalAnimal study (in vivo)Mechanism
In old mice treated with AICAR, improved dilation was independent of nitric oxide or prostaglandin signaling.
In plain wordsIn old mice, improved artery dilation after AICAR did not depend on nitric oxide or prostaglandin signaling.
Peptide
AICAR (acadesine)
Outcome
Not applicableDilation mechanism
Study
mousen: not reported in source
old B6D2F1 mice
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated · 2 weeksAs given in this study (mouse).
Source sentences
Summary
The improvement in EDD was independent of NO or prostaglandin signaling, suggesting enhanced endothelium-dependent hyperpolarizing factor-related dilation.
1 context sentence(design, population, supporting numbers)
Summary · context
Old (28-30 months) B6D2F1 mice had reduced arterial AMPK expression and superoxide-mediated suppression of EDD vs. young (3-6 months) controls.
Report a problemFND-2248414603

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

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.

Publication types

MeSH terms

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