成体心脏自我修复的最新报道

pujixing

nature letter
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6 ~3 ~1 n% w3 X6 Q. `& vDe novo cardiomyocytes from within the activated  g! z* ~! ?# {2 d2 c: ?0 @
adult heart after injury- J0 @6 H/ f# T9 i
Nicola Smart1*, Sveva Bollini1*, Karina N. Dube´1, Joaquim M. Vieira1, Bin Zhou2,3,4, Sean Davidson5, Derek Yellon5,' y7 e# Q4 d# p/ D
Johannes Riegler6,7, Anthony N. Price8, Mark F. Lythgoe6, William T. Pu2,3 & Paul R. Riley1
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; x& R9 M& g8 PA significant bottleneck in cardiovascular regenerative medicine is: T) M6 _% F' C: M# f
the identification of a viable source of stem/progenitor cells that9 u0 b6 R: ], n0 W5 _
could contribute new muscle after ischaemic heart disease and
0 V0 k+ k6 [6 B' s8 z4 W- p% \acute myocardial infarction1. A therapeutic ideal—relative to cell* X! d' u. \4 @2 R. l; i( z
transplantation—would be to stimulate a resident source, thus# }3 E9 i5 A: x3 ~4 @6 j' u9 D
avoiding the caveats of limited graft survival, restricted homing
4 A1 `# n4 {% |" n2 J, Pto the site of injury and host immune rejection. Here we demonstrate
8 Y3 ]/ [4 H4 n0 T6 i, Xin mice that the adult heart contains a resident stem or
& i. L5 O" c/ W0 F9 _progenitor cell population, which has the potential to contribute
6 v1 K1 J$ c' e* G* }3 G3 R/ Vbona fide terminally differentiated cardiomyocytes after myocardial) `3 j- W8 v( h
infarction. We reveal a novel genetic label of the activated
  ]. j, [5 H* ~& o5 D2 ?adult progenitors via re-expression of a key embryonic epicardial# `7 N2 g, d; b& g& \' K
gene, Wilm’s tumour 1 (Wt1), through priming by thymosin b4, a
/ g9 V% ~) ?+ b4 u" h# Ppeptide previously shown to restore vascular potential to adult- E5 U  V' e9 H/ U
epicardium-derived progenitor cells2 with injury. Cumulative
/ r7 G+ u$ G+ u, ]9 R) p2 b& vevidence indicates an epicardial origin of the progenitor population,
/ K: [) s6 Y( cand embryonic reprogramming results in the mobilization
+ p* c: I9 X6 P4 U' _of this population and concomitant differentiation to give rise to de1 t+ u0 q5 M1 x
novo cardiomyocytes. Cell transplantation confirmed a progenitor: f1 A9 V& g, E2 h9 Q" E8 F8 i' X" r
source and chromosome painting of labelled donor cells revealed$ Z0 j- P5 h  q. u4 ]4 b
transdifferentiation to a myocyte fate in the absence of cell fusion.
4 O/ j/ J& |6 s2 K4 ?+ _Derived cardiomyocytes are shown here to structurally and functionally
1 X) u  s2 r+ K: a  q) k: vintegrate with resident muscle; as such, stimulation of this1 U2 ~' P( s- ?" K- R" W% r' q
adult progenitor pool represents a significant step towards residentcell-
5 P$ f1 j, O# g( lbased therapy in human ischaemic heart disease.

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严格说应该叫（通过）外源性刺激激活心脏损伤内源性修复机制

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