Role of Chitinase-3-like Protein 1 in Cardioprotection and Angiogenesis by Post-Infarction Exercise Training.

Li Z, Wu F, Xi L, Tian Z

Biomedicines29 Apr 2022Cited by 7 (Europe PMC)

PMID35625766PMCIDPMC9138221DOI10.3390/biomedicines10051028PepBankPUB-35625766

Summary

Chitinase-3-like protein 1 (CHI3L1) is a myokine involving tissue remodeling and inflammatory processes. CHI3L1 and its receptor protease-activated receptor 2 (PAR2) are induced by exercise in skeletal muscles. However, it remains unknown if CHI3L1/PAR2 signaling also mediates exercise-induced cardioprotection after myocardial infarction. Twenty-four adult male rats were divided into three groups (n = 8/group), receiving: (1) a sham operation; (2) permanent ligation of left anterior descending coronary artery; and (3) post-MI exercise training with one-week adaptive treadmill exercise for seven days followed by four weeks of aerobic exercise. Left ventricular systolic and end-diastolic pressure indices were measured and cardiac fibrosis, and angiogenesis were examined. Furthermore, HUVEC cells were treated in vitro with AMPK agonist-AICAR (a putative pharmacological memetic of exercise), recombinant human CHI3L1, PAR2 receptor blocker (AZ3451), and PI3K inhibitor (LY294002), respectively. We found that post-MI exercise significantly upregulated CHI3L1, PAR2, pPI3K/PI3K, pAKT/AKT, pERK/ERK, improved cardiac function, and diminished fibrosis. AICAR increased HUVEC tubules formation and upregulated CHI3L1 and PAR2 and these changes were attenuated by PAR2 blocker. In conclusion, post-MI exercise training can effectively activate CHI3L1/PAR2 signaling, which led to the improved myocardial function and enhanced cardiac angiogenesis in the infarcted heart.

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

Results from this study3

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

01LabIn vitro (cells)Mechanism
In HUVEC cells, AICAR increased tubule formation, and a PAR2 blocker attenuated this change.
In plain wordsIn cells, AICAR increased vessel-like tube formation, and a PAR2 blocker weakened this change.
Peptide
AICAR (acadesine)
Outcome
IncreaseTubule formation
Study
n: not reported in source
HUVEC cells
Outcome group
Angiogenesis · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
AICAR increased HUVEC tubules formation and upregulated CHI3L1 and PAR2 and these changes were attenuated by PAR2 blocker.
1 context sentence(design, population, supporting numbers)
Summary · context
Furthermore, HUVEC cells were treated in vitro with AMPK agonist-AICAR (a putative pharmacological memetic of exercise), recombinant human CHI3L1, PAR2 receptor blocker (AZ3451), and PI3K inhibitor (LY294002), respectively.
Show in the study text Report a problemFND-3562576601
02LabIn vitro (cells)Mechanism
In HUVEC cells, AICAR upregulated CHI3L1, and a PAR2 blocker attenuated this change.
In plain wordsIn cells, AICAR increased CHI3L1, and a PAR2 blocker weakened this change.
Peptide
AICAR (acadesine)
Outcome
IncreaseCHI3L1 expression
Study
n: not reported in source
HUVEC cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
AICAR increased HUVEC tubules formation and upregulated CHI3L1 and PAR2 and these changes were attenuated by PAR2 blocker.
1 context sentence(design, population, supporting numbers)
Summary · context
Furthermore, HUVEC cells were treated in vitro with AMPK agonist-AICAR (a putative pharmacological memetic of exercise), recombinant human CHI3L1, PAR2 receptor blocker (AZ3451), and PI3K inhibitor (LY294002), respectively.
Show in the study text Report a problemFND-3562576602
03LabIn vitro (cells)Mechanism
In HUVEC cells, AICAR upregulated PAR2, and a PAR2 blocker attenuated this change.
In plain wordsIn cells, AICAR increased PAR2, and a PAR2 blocker weakened this change.
Peptide
AICAR (acadesine)
Outcome
IncreasePAR2 expression
Study
n: not reported in source
HUVEC cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
AICAR increased HUVEC tubules formation and upregulated CHI3L1 and PAR2 and these changes were attenuated by PAR2 blocker.
1 context sentence(design, population, supporting numbers)
Summary · context
Furthermore, HUVEC cells were treated in vitro with AMPK agonist-AICAR (a putative pharmacological memetic of exercise), recombinant human CHI3L1, PAR2 receptor blocker (AZ3451), and PI3K inhibitor (LY294002), respectively.
Show in the study text Report a problemFND-3562576603

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

Keywords

PepBank is a research reference. Talk to a doctor before you use any peptide.