ライフサイエンスコーパス: liver repair

1 are injury models that favor stem cell-based liver repair.

2 in BM-MSCs all led to increased efficacy for liver repair.

3 isingly exacerbated liver injury and delayed liver repair.

4 mmatory and anti-fibrotic actions to enhance liver repair.

5 complex signaling network that orchestrates liver repair.

6 are targets of injury, but also orchestrate liver repair.

7 ors but impaired monocyte recruitment during liver repair.

8 n-1 influences later mechanisms that lead to liver repair.

9 id-specific Foxm1 deletion caused a delay in liver repair.

10 hepatic MMPs are responsible for successful liver repair.

11 rarely and contribute to a lesser extent to liver repair.

12 tor (G-CSF) may be effective in facilitating liver repair.

13 cell reaction, and the contribution of BM to liver repair.

14 ic liver injury in humans, is a regulator of liver repair.

15 rokinase-type plasminogen activator (uPA) in liver repair.

16 ince been determined to be very important in liver repair.

17 at generate factors that promote maladaptive liver repair.

18 potentially reversible, particularly during liver repair.

19 on for the strategies for vasculature-driven liver repair.

20 uting to the resolution of inflammation, and liver repair.

21 ndogenous stem/progenitors to participate in liver repair.

22 onocyte-derived macrophages are critical for liver repair after acetaminophen (APAP) overdose.

23 ype 2 macrophage activation was required for liver repair after bacterial infection, but resulted in

24 Complement has been implicated in liver repair after toxic injury.

25 n that factors released by MSCs could induce liver repair and ameliorate systemic inflammation throug

26 The role of progenitor cells in liver repair and fibrosis has been extensively described

27 cells (HPCs), regulating the balance between liver repair and fibrosis.

28 s hematopoietic stem cells (HSCs) can aid in liver repair and improve survival in an animal model of

29 Foxm1 is critical for liver repair and is required for the recruitment of mono

30 the difference between healthy regenerative liver repair and pathologic repair.

31 that MSCs are a valuable source of cells for liver repair and regeneration and that, by the alteratio

32 The process of liver repair and regeneration following hepatic injury i

33 es play important roles in the mechanisms of liver repair and regeneration through their effects on h

34 data suggest that TNF-alpha participates in liver repair and regeneration, in part, by directly indu

35 progenitor cells (HPCs) play a major role in liver repair and regeneration.

36 f monocytes to Foxm1-deficient mice restored liver repair and rescued liver function.

37 We suggest that AhR may serve to adjust liver repair and to block tumorigenesis by modulating st

38 e cells (HpSC), well known to participate in liver repairing and fibrosis, mediate potent immunomodul

39 activation markers Ym1 and Fizz1, increased liver repair, and reduced hepatotoxicity.

40 nase activity and collagen resorption during liver repair, and speculate that PMN-derived MMP8 or PMN

41 mice deleted for Il11 exhibited spontaneous liver repair but HyperIl6, despite robustly activating S

42 an-1 HS halt disease progression and promote liver repair by enhancing hepatocyte survival in AILI.

43 the fate of key cell types involved in adult liver repair by modulating epithelial-to-mesenchymal-lik

44 onclusion, Foxf1 +/- mice exhibited abnormal liver repair, diminished activation of hepatic stellate

45 ervations indicated that YAP was crucial for liver repair during alcohol-associated injury.

46 To evaluate this possibility, we examined liver repair during different types of liver injury afte

47 e report a potential role of beta-catenin in liver repair, especially in enhancing the resolution of

48 revealed unanticipated roles of p75(NTR) in liver repair, fibrinolysis, lung fibrosis, muscle regene

49 extracellular matrix, we examined Foxf1 +/- liver repair following carbon tetrachloride injury, a kn

50 Molecular mechanisms regulating liver repair following cholestatic injury remain largely

51 ess in multiple organ systems and influences liver repair following hepatotoxic damage or regeneratio

52 ors regulating cellular proliferation during liver repair have been identified, the mechanisms by whi

53 es a mechanistic-based therapy for promoting liver repair in aging.

54 Here, we investigated whether the defective liver repair in mice lacking Plg is due to impaired acti

55 rrected the functional deficits and improved liver repair in Plg-deficient mice.

56 lso correlated significantly with markers of liver repair, including numbers of hepatic progenitors a

57 Liver repair involves phenotypic changes in hepatic stel

58 cirrhosis, a disabling outcome of defective liver repair, involves deregulated accumulation of myofi

59 Antibody treatment slightly delayed liver repair processes, as evidenced by extending the pe

60 potentiating hepatotoxicity and/or aiding in liver repair processes.

61 with stem-like properties that contribute to liver repair/regeneration under different pathophysiolog

62 s; however, the mechanisms and potential for liver repair remain unclear.

63 ly modulate regeneration and fibrosis during liver repair remains to be defined.

64 While hepatic inflammation is critical for liver repair, the transcriptional mechanisms required fo

65 Because this has potential implications for liver repair, this review will summarize current knowled

66 ontribute to liver injury, it may also block liver repair through inhibition of hepatocyte proliferat

67 q+) MoMFs that promoted necrotic removal and liver repair, while Pdgfb+ MoMFs activated hepatic stell

68 blocking VEGF receptors abrogates BEC-driven liver repair, while VEGFA overexpression promotes it.