Connection

Michael Zile to Mice, Inbred C57BL

This is a "connection" page, showing publications Michael Zile has written about Mice, Inbred C57BL.
Connection Strength

0.453
  1. In vivo measurements of the contributions of protein synthesis and protein degradation in regulating cardiac pressure overload hypertrophy in the mouse. Mol Cell Biochem. 2012 Aug; 367(1-2):205-13.
    View in: PubMed
    Score: 0.062
  2. Pressure overload-induced alterations in fibrillar collagen content and myocardial diastolic function: role of secreted protein acidic and rich in cysteine (SPARC) in post-synthetic procollagen processing. Circulation. 2009 Jan 20; 119(2):269-80.
    View in: PubMed
    Score: 0.049
  3. Mechanisms that limit regression of myocardial fibrosis following removal of left ventricular pressure overload. Am J Physiol Heart Circ Physiol. 2022 07 01; 323(1):H165-H175.
    View in: PubMed
    Score: 0.031
  4. The prevalent I686T human variant and loss-of-function mutations in the cardiomyocyte-specific kinase gene TNNI3K cause adverse contractility and concentric remodeling in mice. Hum Mol Genet. 2021 01 06; 29(21):3504-3515.
    View in: PubMed
    Score: 0.028
  5. SPARC production by bone marrow-derived cells contributes to myocardial fibrosis in pressure overload. Am J Physiol Heart Circ Physiol. 2021 02 01; 320(2):H604-H612.
    View in: PubMed
    Score: 0.028
  6. Pressure overload generates a cardiac-specific profile of inflammatory mediators. Am J Physiol Heart Circ Physiol. 2020 08 01; 319(2):H331-H340.
    View in: PubMed
    Score: 0.027
  7. Elevated Wall Tension Leads to Reduced miR-133a in the Thoracic Aorta by Exosome Release. J Am Heart Assoc. 2019 01 08; 8(1):e010332.
    View in: PubMed
    Score: 0.025
  8. Increased macrophage-derived SPARC precedes collagen deposition in myocardial fibrosis. Am J Physiol Heart Circ Physiol. 2018 07 01; 315(1):H92-H100.
    View in: PubMed
    Score: 0.023
  9. Cardiac macrophages promote diastolic dysfunction. J Exp Med. 2018 02 05; 215(2):423-440.
    View in: PubMed
    Score: 0.023
  10. Increased ADAMTS1 mediates SPARC-dependent collagen deposition in the aging myocardium. Am J Physiol Endocrinol Metab. 2016 06 01; 310(11):E1027-35.
    View in: PubMed
    Score: 0.020
  11. Lactosylceramide contributes to mitochondrial dysfunction in diabetes. J Lipid Res. 2016 Apr; 57(4):546-62.
    View in: PubMed
    Score: 0.020
  12. Suppressing angiotensinogen synthesis attenuates kidney cyst formation in a Pkd1 mouse model. FASEB J. 2016 Jan; 30(1):370-9.
    View in: PubMed
    Score: 0.020
  13. Secreted protein acidic and rich in cysteine facilitates age-related cardiac inflammation and macrophage M1 polarization. Am J Physiol Cell Physiol. 2015 Jun 15; 308(12):C972-82.
    View in: PubMed
    Score: 0.019
  14. ?3 integrin in cardiac fibroblast is critical for extracellular matrix accumulation during pressure overload hypertrophy in mouse. PLoS One. 2012; 7(9):e45076.
    View in: PubMed
    Score: 0.016
  15. Effects of the absence of procollagen C-endopeptidase enhancer-2 on myocardial collagen accumulation in chronic pressure overload. Am J Physiol Heart Circ Physiol. 2012 Jul 15; 303(2):H234-40.
    View in: PubMed
    Score: 0.016
  16. Calpain inhibition preserves myocardial structure and function following myocardial infarction. Am J Physiol Heart Circ Physiol. 2009 Nov; 297(5):H1744-51.
    View in: PubMed
    Score: 0.013
  17. Beta3 integrin-mediated ubiquitination activates survival signaling during myocardial hypertrophy. FASEB J. 2009 Aug; 23(8):2759-71.
    View in: PubMed
    Score: 0.013
  18. A multidimensional proteomic approach to identify hypertrophy-associated proteins. Proteomics. 2006 Apr; 6(7):2225-35.
    View in: PubMed
    Score: 0.010
  19. Role of microtubules versus myosin heavy chain isoforms in contractile dysfunction of hypertrophied murine cardiocytes. Am J Physiol Heart Circ Physiol. 2003 Sep; 285(3):H1270-85.
    View in: PubMed
    Score: 0.008
Connection Strength

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Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.