Evidence map›Paper›PMID 25980021›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Hyperhomocysteinemia inhibits satellite cell regenerative capacity through p38 alpha/beta MAPK signaling.

Sudhakar Veeranki, David Lominadze, Suresh C Tyagi

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Cystathionine β-synthase regulates mitochondrial morphogenesis in ovarian cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  14. Pentosidine concentration is associated with degenerative lumbar scoliosis in older women: preliminary results.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2018
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

Sudhakar VeerankiDepartment of Physiology and Biophysics, University of Louisville, Louisville, Kentucky s0veer02@louisville.edu.
David LominadzeDepartment of Physiology and Biophysics, University of Louisville, Louisville, Kentucky.
Suresh C TyagiDepartment of Physiology and Biophysics, University of Louisville, Louisville, Kentucky.
University of Louisville · US

Funding

Reversing diabetic muscle myopathy by exercise and exosomesR01HL074185 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2003 to 2018
$5.7M
Mechanisms of plasticity and repair after SCIP30GM103507 · NIGMS · UNIVERSITY OF LOUISVILLE · PI WHITTEMORE, SCOTT R · 2012 to 2015
$4.2M
Mechanism of Vascular Remodeling in HyperhomocysteinemiaR01HL071010 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI TYAGI, SURESH C. · 2002 to 2010
$2.7M
Mechanisms of Homocysteine-Induced Fibrinogen-Amyloid Plaque FormationR01NS084823 · NINDS · UNIVERSITY OF LOUISVILLE · PI LOMINADZE, DAVID, TYAGI, SURESH C. · 2013 to 2017
$2.7M
Hydrogen sulfide mechanism of renal hypertensionR01DK104653 · NIDDK · UNIVERSITY OF LOUISVILLE · PI SEN, UTPAL, TYAGI, SURESH C. · 2015 to 2018
$2.5M
Mitophagic and anti-angiogenic mechanism of heart failureR01HL108621 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2011 to 2015
$1.8M
Mechanisms of Cerebral Vascular RemodelingR01NS051568 · NINDS · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2007 to 2011
$1.6M
NHLBI NIH HHS HL-108621NHLBI NIH HHS HL-74185NHLBI NIH HHS R01 HL071010NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL108621NIGMS NIH HHS P30 GM103507NINDS NIH HHS NS-84823NINDS NIH HHS R01 NS051568NINDS NIH HHS R01 NS084823
6 · The paper itself

Abstract

Chronic failure in maintenance and regeneration of skeletal muscles leads to lower muscle mass (sarcopenia), muscle weakness, and poor response to injury. Evidence suggests that aberrant p38 MAPK signaling undermines the repair process after injury in aged mice. Previous studies have shown that hyperhomocysteinemia (HHcy) has been associated with muscle weakness and lower than normal body weights. However, whether or not HHcy condition also compromises skeletal muscle regenerative capabilities is not clear. In the current study, we show that CBS-/+ mice, a model for HHcy condition, exhibited compromised regenerative function and cell proliferation upon injury. However, there was no significant difference in Pax7 expression levels in the satellite cells from CBS-/+ mouse skeletal muscles. Interestingly, the satellite cells from CBS-/+ mice not only exhibited diminished in vitro proliferative capabilities, but also there was heightened oxidative stress. In addition, there was enhanced p38 MAPK activation as well as p16 and p21 expression in the CBS-/+ mouse satellite cells. Moreover, the C2C12 myoblasts also exhibited higher p38 MAPK activation and p16 expression upon treatment with homocysteine in addition to enhanced ROS presence. Tissue engraftment potential and regeneration after injury were restored to some extent upon treatment with the p38-MAPK inhibitor, SB203580, in the CBS-/+ mice. These results together suggest that HHcy-induced diminished satellite cell proliferation involves excessive oxidative stress and p38 MAPK signaling. Our study further proposes that HHcy is a potential risk factor for elderly frailty, and need to be considered as a therapeutic target while designing the alleviation interventions/postinjury rehabilitation measures for adults with HHcy.

Indexed as

Cell ProliferationMAP Kinase Signaling SystemRegenerationAnimalsCell LineCystathionine beta-SynthaseDisease Models, AnimalEnzyme ActivationHyperhomocysteinemiaMice, Inbred C57BLMice, KnockoutMuscle, SkeletalOxidative Stressp38 Mitogen-Activated Protein KinasesPhosphorylationProtein Kinase InhibitorsCystathionine beta-Synthasep38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReactive Oxygen SpeciesCBShyperhomocysteinemiap16p21p38 MAPKreactive oxygen speciesskeletal muscle

Identifiers

PMID25980021
PMCPMC4504963
OpenAlexW2119316488

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.