2008
DOI: 10.1016/j.jacc.2008.01.011
|View full text |Cite
|
Sign up to set email alerts
|

Aging-Related Defects Are Associated With Adverse Cardiac Remodeling in a Mouse Model of Reperfused Myocardial Infarction

Abstract: Although young mice exhibit a robust post-infarction inflammatory response and form dense collagenous scars, senescent mice show suppressed inflammation, delayed granulation tissue formation, and markedly reduced collagen deposition. These defects might contribute to adverse remodeling. These observations suggest that caution is necessary when attempting to therapeutically target the post-infarction inflammatory response in patients with reperfused MI. The injurious potential of inflammatory mediators might ha… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

7
155
3

Year Published

2010
2010
2019
2019

Publication Types

Select...
4
2

Relationship

1
5

Authors

Journals

citations
Cited by 177 publications
(166 citation statements)
references
References 31 publications
7
155
3
Order By: Relevance
“…Consequently, myofibroblasts from aged heart express less ␣-SMA ( Figure 3C), in agreement with the findings of Bujak et al, 7 who demonstrated decreased myofibroblast accumulation in the aged infarcted myocardium. Even with a noticeable lack of FAK, Tak1, p38MAPK, and JNK phosphorylation in response to 30 minutes of stimulation with TGF-␤1 observed in fibroblasts isolated from aged mice (Figure 3, E-G, and Figure 7A), the pharmacologic inhibition of Tak1, p38MAPK, or JNK resulted in abolished TGF-␤1-mediated contraction of free-floating collagen pads ( Figure 7, C and E; see also Supplemental Figure S6 at http://ajp.amjpathol.org), which suggests that these pathways are still important for fibroblasts isolated from aged mice, and perhaps their activation kinetics is different from that in fibroblasts isolated from young mice.…”
Section: Discussionsupporting
confidence: 92%
See 4 more Smart Citations
“…Consequently, myofibroblasts from aged heart express less ␣-SMA ( Figure 3C), in agreement with the findings of Bujak et al, 7 who demonstrated decreased myofibroblast accumulation in the aged infarcted myocardium. Even with a noticeable lack of FAK, Tak1, p38MAPK, and JNK phosphorylation in response to 30 minutes of stimulation with TGF-␤1 observed in fibroblasts isolated from aged mice (Figure 3, E-G, and Figure 7A), the pharmacologic inhibition of Tak1, p38MAPK, or JNK resulted in abolished TGF-␤1-mediated contraction of free-floating collagen pads ( Figure 7, C and E; see also Supplemental Figure S6 at http://ajp.amjpathol.org), which suggests that these pathways are still important for fibroblasts isolated from aged mice, and perhaps their activation kinetics is different from that in fibroblasts isolated from young mice.…”
Section: Discussionsupporting
confidence: 92%
“…6,7 Mesenchymal progenitor cells have been identified as a potential fibroblast source, 8,10 and recent evidence suggests they may contribute to cardiac tissue repair by differentiating to scarforming myofibroblasts. 49 As demonstrated herein, those cardiac MSCs are positive for CD44, Nanog, and Oct3/4, and are multipotential.…”
Section: Discussionmentioning
confidence: 99%
See 3 more Smart Citations