Evidence map›Paper›PMID 23825069›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Increasing cGMP-dependent protein kinase I activity attenuates cisplatin-induced kidney injury through protection of mitochondria function.

Hasiyeti Maimaitiyiming, Yanzhang Li, Wenpeng Cui, Xiaopeng Tong, Heather Norman, Xinyu Qi, Shuxia Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 42 citations in OpenAlex.

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  5. Depletion of cyclic-GMP levels and inhibition of cGMP-dependent protein kinase activate p21FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hasiyeti MaimaitiyimingGraduate Center for Nutritional Sciences, Univ. of Kentucky, Wethington Bldg. Rm. 583, 900 S. Limestone St., Lexington, KY 40536. swang7@uky.edu.
Yanzhang Li
Wenpeng Cui
Xiaopeng Tong
Heather Norman
Xinyu Qi
Shuxia Wang
University of Kentucky · US

Funding

TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
Upstream Stimulatory Factor 2 regulation of renin in diabetic nephropathyR01DK081555 · NIDDK · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2009 to 2013
$1.3M
Thrombospondin 1 in obesity associated inflammation and insulin resistanceR01DK098176 · NIDDK · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2014 to 2017
$1.2M
NIDDK NIH HHS DK-081555NIDDK NIH HHS R01 DK081555NIDDK NIH HHS R01 DK098176NIDDK NIH HHS T32 DK007778
6 · The paper itself

Abstract

Cisplatin is widely used to treat malignancies. However, its major limitation is the development of dose-dependent nephrotoxicity. The precise mechanisms of cisplatin-induced kidney damage remain unclear, and the renoprotective agents during cisplatin treatment are still lacking. Here, we demonstrated that the expression and activity of cGMP-dependent protein kinase-I (PKG-I) were reduced in cisplatin-treated renal tubular cells in vitro as well as in the kidney tissues from cisplatin-treated mice in vivo. Increasing PKG activity by both pharmacological and genetic approaches attenuated cisplatin-induced kidney cell apoptosis in vitro. This was accompanied by decreased Bax/Bcl2 ratio, caspase 3 activity, and cytochrome c release. Cisplatin-induced mitochondria membrane potential loss in the tubular cells was also prevented by increased PKG activity. All of these data suggest a protective effect of PKG on mitochondria function in renal tubular cells. Importantly, increasing PKG activity pharmacologically or genetically diminished cisplatin-induced tubular damage and preserved renal function during cisplatin treatment in vivo. Mitochondria structural and functional damage in the kidney from cisplatin-treated mice was inhibited by increased PKG activity. In addition, increasing PKG activity enhanced ciaplatin-induced cell death in several cancer cell lines. Taken together, these results suggest that increasing PKG activity may be a novel option for renoprotection during cisplatin-based chemotherapy.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCell LineCisplatinCyclic GMP-Dependent Protein Kinase Type IDown-RegulationHumansKidneyKidney Tubules, ProximalMaleMiceMice, TransgenicMitochondriaCisplatinCyclic GMP-Dependent Protein Kinase Type IcisplatinmitochondriaPKG-Itubular cells

Identifiers

PMID23825069
PMCPMC3761289
OpenAlexW2075161839

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.