RGD Reference Report - Mitochondrial damage: an important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats. - Rat Genome Database

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Mitochondrial damage: an important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats.

Authors: Li, Ruijin  Kou, Xiaojing  Geng, Hong  Xie, Jingfang  Tian, Jingjing  Cai, Zongwei  Dong, Chuan 
Citation: Li R, etal., J Hazard Mater. 2015 Apr 28;287:392-401. doi: 10.1016/j.jhazmat.2015.02.006. Epub 2015 Feb 4.
RGD ID: 12437078
Pubmed: PMID:25677476   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jhazmat.2015.02.006   (Journal Full-text)

Epidemiological studies suggested that ambient fine particulate matter (PM2.5) exposure was associated with cardiovascular disease. However, the underlying mechanism, especially the mitochondrial damage mechanism, of PM2.5-induced heart acute injury is still unclear. In this study, the alterations of mitochondrial morphology and mitochondrial fission/fusion gene expression, oxidative stress, calcium homeostasis and inflammation in hearts of rats exposed to PM2.5 with different dosages (0.375, 1.5, 6.0 and 24.0mg/kg body weight) were investigated. The results indicated that the PM2.5 exposure induced pathological changes and ultra-structural damage in hearts such as mitochondrial swell and cristae disorder. Furthermore, PM2.5 exposure significantly increased specific mitochondrial fission/fusion gene (Fis1, Mfn1, Mfn2, Drp1 and OPA1) expression in rat hearts. These changes were accompanied by decreases of activities of superoxide dismutase (SOD), Na(+)K(+)-ATPase and Ca(2+)-ATPase and increases of levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) as well as levels of pro-inflammatory mediators including TNF-α, IL-6 and IL-1ß in rat hearts. The results implicate that mitochondrial damage, oxidative stress, cellular homeostasis imbalance and inflammation are potentially important mechanisms for the PM2.5-induced heart injury, and may have relations with cardiovascular disease.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Acute Heart Injury  ISOMfn1 (Rattus norvegicus)12437078; 12437078mRNA and protein:increased expression:heart (rat)RGD 
Acute Heart Injury  IEP 12437078mRNA and protein:increased expression:heart (rat)RGD 
Heart Injuries  ISOFis1 (Rattus norvegicus)12437078; 12437078mRNA and protein:increased expression:heart (rat)RGD 
Heart Injuries  IEP 12437078; 12437078mRNA and protein:increased expression:heart (rat)RGD 
Heart Injuries  ISOOpa1 (Rattus norvegicus)12437078; 12437078mRNA and protein:increased expression:heart (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Fis1  (fission, mitochondrial 1)
Mfn1  (mitofusin 1)
Opa1  (OPA1, mitochondrial dynamin like GTPase)

Genes (Mus musculus)
Fis1  (fission, mitochondrial 1)
Mfn1  (mitofusin 1)
Opa1  (OPA1, mitochondrial dynamin like GTPase)

Genes (Homo sapiens)
FIS1  (fission, mitochondrial 1)
MFN1  (mitofusin 1)
OPA1  (OPA1 mitochondrial dynamin like GTPase)


Additional Information