成体心脏自我修复的最新报道

pujixing

nature letter
. e8 u+ h( {* g8 W
) @9 V/ M+ ^- y) D7 R. y6 U% p3 IDe novo cardiomyocytes from within the activated
* m5 y* f& J1 A1 q5 hadult heart after injury+ S& S9 f$ ?# g  e) k, D6 p0 k6 f
Nicola Smart1*, Sveva Bollini1*, Karina N. Dube´1, Joaquim M. Vieira1, Bin Zhou2,3,4, Sean Davidson5, Derek Yellon5,
' j+ T, y" v, N/ j. @8 o3 PJohannes Riegler6,7, Anthony N. Price8, Mark F. Lythgoe6, William T. Pu2,3 & Paul R. Riley1
+ f) t) v3 j( }. Y! ~" \" e3 N/ W: G; {; j( Q$ q$ V1 D
A significant bottleneck in cardiovascular regenerative medicine is
! E  l/ o8 w, T& U! S! j; Zthe identification of a viable source of stem/progenitor cells that
2 b) A- ^  ?' E4 Y, M2 ccould contribute new muscle after ischaemic heart disease and
& p+ K& Z9 B' j  ^- u) g' N3 _' Uacute myocardial infarction1. A therapeutic ideal—relative to cell
& S, j, i7 u/ P1 [transplantation—would be to stimulate a resident source, thus+ d( [6 _3 Y" r! e% ]
avoiding the caveats of limited graft survival, restricted homing
' `7 |, F/ a4 {' D* q# Ito the site of injury and host immune rejection. Here we demonstrate
/ O* O! D/ S  `& _# Xin mice that the adult heart contains a resident stem or+ @6 _6 I7 X# e  S: o
progenitor cell population, which has the potential to contribute
, |% z" n! ?' J- W: Fbona fide terminally differentiated cardiomyocytes after myocardial
4 e2 U( H  G  P/ @0 L8 l# ?infarction. We reveal a novel genetic label of the activated
1 x8 c0 n$ `# }, h" |) S* f" Xadult progenitors via re-expression of a key embryonic epicardial3 C8 m4 R3 I* D5 O0 r; q
gene, Wilm’s tumour 1 (Wt1), through priming by thymosin b4, a  U2 U2 u9 v' n" |6 J3 y- r
peptide previously shown to restore vascular potential to adult+ u) Y" Q; P$ m) T- P1 R7 y. G( Y
epicardium-derived progenitor cells2 with injury. Cumulative
/ Z: u4 {5 j: ~/ c& z- {" r) ]7 _4 V3 [evidence indicates an epicardial origin of the progenitor population,
( |+ f) T  j, t3 a' E2 oand embryonic reprogramming results in the mobilization" f2 w4 T* _/ |7 \1 u
of this population and concomitant differentiation to give rise to de
. D% S6 ?2 r1 `' x$ x4 F. anovo cardiomyocytes. Cell transplantation confirmed a progenitor" d" n, K, F8 P4 i9 H
source and chromosome painting of labelled donor cells revealed7 S$ A! P" D& F' s9 ~& m
transdifferentiation to a myocyte fate in the absence of cell fusion.5 _9 N: m  J+ s4 b4 G. P+ }; M
Derived cardiomyocytes are shown here to structurally and functionally
' C- ~3 O7 J7 h. r. Tintegrate with resident muscle; as such, stimulation of this( Q4 m) }( M# ~1 M) {1 @
adult progenitor pool represents a significant step towards residentcell-
& R# [2 P1 G4 Y! F( ^; T: }based therapy in human ischaemic heart disease.

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- \( `- g0 D, D+ A( U+ S6 B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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