(Q50457515)

English

Recruitment and subsequent proliferation of bone marrow-derived cells in the postischemic kidney are important to the progression of fibrosis.

scientific article published on 16 April 2014

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

Recruitment and subsequent proliferation of bone marrow-derived cells in the postischemic kidney are important to the progression of fibrosis. (English)

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

1

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

author name string

Jee In Kim

2

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

Sang Jun Han

3

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

Kwon Moo Park

4

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

publication date

16 April 2014

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

American Journal of Physiology - Renal Physiology

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

306

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

12

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

F1451-61

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

Renal microenvironments and macrophage phenotypes determine progression or resolution of renal inflammation and fibrosis.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Nox4 and nox2 NADPH oxidases mediate distinct cellular redox signaling responses to agonist stimulation

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Effects of NADPH oxidase inhibitor in diabetic nephropathy

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Persistent oxidative stress following renal ischemia-reperfusion injury increases ANG II hemodynamic and fibrotic activity

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Cellular pathophysiology of ischemic acute kidney injury

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Antioxidant intervention blunts renal injury in experimental renovascular disease

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

NADPH oxidase in the liver: defensive, offensive, or fibrogenic?

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Nox-2 is a modulator of fibrogenesis in kidney allografts

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Macrophages and immunologic inflammation of the kidney

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Antibodies against macrophages that overlap in specificity with fibroblasts.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Activation of ERK accelerates repair of renal tubular epithelial cells, whereas it inhibits progression of fibrosis following ischemia/reperfusion injury

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Infiltrated macrophages contribute to recovery after ischemic injury but not to ischemic preconditioning in kidneys

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Bone marrow-derived cells play a major role in kidney fibrosis via proliferation and differentiation in the infiltrated site.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Involvement of hydrogen sulfide and homocysteine transsulfuration pathway in the progression of kidney fibrosis after ureteral obstruction

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Reactive oxygen species differently regulate renal tubular epithelial and interstitial cell proliferation after ischemia and reperfusion injury.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Intra-renal slow cell-cycle cells contribute to the restoration of kidney tubules injured by ischemia/reperfusion

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Macrophages contribute to the development of renal fibrosis following ischaemia/reperfusion-induced acute kidney injury

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Origin and function of myofibroblasts in kidney fibrosis

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

The contribution of bone marrow-derived cells to the development of renal interstitial fibrosis.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Bone marrow Ly6Chigh monocytes are selectively recruited to injured kidney and differentiate into functionally distinct populations.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Pericytes and perivascular fibroblasts are the primary source of collagen-producing cells in obstructive fibrosis of the kidney

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Apocynin attenuates tubular apoptosis and tubulointerstitial fibrosis in transgenic mice independent of hypertension

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Biological roles for the NOX family NADPH oxidases

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Prevention of kidney ischemia/reperfusion-induced functional injury and JNK, p38, and MAPK kinase activation by remote ischemic pretreatment

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Macrophage diversity in renal injury and repair.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

NADPH oxidases, reactive oxygen species, and the kidney: friend and foe.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Advanced oxidation protein products promote inflammation in diabetic kidney through activation of renal nicotinamide adenine dinucleotide phosphate oxidase

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Reactive oxygen species in cell signaling

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

NADPH oxidase 2 regulates bone marrow microenvironment following hindlimb ischemia: role in reparative mobilization of progenitor cells.

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Cellular and molecular mechanisms of fibrosis

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Macrophages: master regulators of inflammation and fibrosis

1 reference

https://api.crossref.org/works/10.1152%2FAJPRENAL.00017.2014

21 January 2018

Identifiers

10.1152/AJPRENAL.00017.2014

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

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1 reference

https://api.fatcat.wiki/v0/release/jajfpcredndn3pdqv3knbwwjma

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PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

14 March 2018

http://europepmc.org/abstract/MED/24740786

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