FAT-free p300 is good for scar-free tissue repair

Asish K Ghosh*

*Corresponding author for this work

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Fibrosis, the deadly pathological manifestation of an abnormal tissue remodeling in any organ due to excessive collagen deposition, is associated with a wide variety of organ failure-related human diseases. Chronic stress or repeated injury in a particular organ induces abnormal molecular signals that lead to super-activation of matrix protein producing fibroblasts, excessive matrix proteins accumulation, loss of physiological tissue architecture or elasticity, and ultimately leading to organ failure. There is no effective therapy for fibrosis. Factor acetyltransferase p300 (FATp300), a major epigenetic regulator that acetylates specific lysines in histones and transcription factors, is essential for elevated collagen synthesis and the levels of FATp300 are significantly elevated in different fibrotic tissues. Pharmacological inhibition of FAT activity of p300 is associated with decreased collagen synthesis by fibroblasts in tissues and amelioration of organ fibrosis. Therefore, FAT-free p300 is superior for physiological tissue repair and must be exploited as a viable therapeutic target against multi-organ fibrosis. J. Cell. Biochem. 115: 1486-1489, 2014.

Original languageEnglish (US)
Pages (from-to)1486-1489
Number of pages4
JournalJournal of Cellular Biochemistry
Volume115
Issue number9
DOIs
StatePublished - Jan 1 2014

Fingerprint

Cicatrix
Repair
Tissue
Fibrosis
Collagen
Fibroblasts
Elasticity
Epigenomics
Histones
Lysine
Proteins
Transcription Factors
Chemical activation
Pharmacology
Wounds and Injuries
Therapeutics
p300-CBP-associated factor

Keywords

  • COLLAGENS
  • EPIGENETICS
  • FIBROBLASTS
  • ORGAN FIBROSIS
  • TISSUE REPAIR
  • p300

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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title = "FAT-free p300 is good for scar-free tissue repair",
abstract = "Fibrosis, the deadly pathological manifestation of an abnormal tissue remodeling in any organ due to excessive collagen deposition, is associated with a wide variety of organ failure-related human diseases. Chronic stress or repeated injury in a particular organ induces abnormal molecular signals that lead to super-activation of matrix protein producing fibroblasts, excessive matrix proteins accumulation, loss of physiological tissue architecture or elasticity, and ultimately leading to organ failure. There is no effective therapy for fibrosis. Factor acetyltransferase p300 (FATp300), a major epigenetic regulator that acetylates specific lysines in histones and transcription factors, is essential for elevated collagen synthesis and the levels of FATp300 are significantly elevated in different fibrotic tissues. Pharmacological inhibition of FAT activity of p300 is associated with decreased collagen synthesis by fibroblasts in tissues and amelioration of organ fibrosis. Therefore, FAT-free p300 is superior for physiological tissue repair and must be exploited as a viable therapeutic target against multi-organ fibrosis. J. Cell. Biochem. 115: 1486-1489, 2014.",
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FAT-free p300 is good for scar-free tissue repair. / Ghosh, Asish K.

In: Journal of Cellular Biochemistry, Vol. 115, No. 9, 01.01.2014, p. 1486-1489.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Ghosh, Asish K

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Fibrosis, the deadly pathological manifestation of an abnormal tissue remodeling in any organ due to excessive collagen deposition, is associated with a wide variety of organ failure-related human diseases. Chronic stress or repeated injury in a particular organ induces abnormal molecular signals that lead to super-activation of matrix protein producing fibroblasts, excessive matrix proteins accumulation, loss of physiological tissue architecture or elasticity, and ultimately leading to organ failure. There is no effective therapy for fibrosis. Factor acetyltransferase p300 (FATp300), a major epigenetic regulator that acetylates specific lysines in histones and transcription factors, is essential for elevated collagen synthesis and the levels of FATp300 are significantly elevated in different fibrotic tissues. Pharmacological inhibition of FAT activity of p300 is associated with decreased collagen synthesis by fibroblasts in tissues and amelioration of organ fibrosis. Therefore, FAT-free p300 is superior for physiological tissue repair and must be exploited as a viable therapeutic target against multi-organ fibrosis. J. Cell. Biochem. 115: 1486-1489, 2014.

AB - Fibrosis, the deadly pathological manifestation of an abnormal tissue remodeling in any organ due to excessive collagen deposition, is associated with a wide variety of organ failure-related human diseases. Chronic stress or repeated injury in a particular organ induces abnormal molecular signals that lead to super-activation of matrix protein producing fibroblasts, excessive matrix proteins accumulation, loss of physiological tissue architecture or elasticity, and ultimately leading to organ failure. There is no effective therapy for fibrosis. Factor acetyltransferase p300 (FATp300), a major epigenetic regulator that acetylates specific lysines in histones and transcription factors, is essential for elevated collagen synthesis and the levels of FATp300 are significantly elevated in different fibrotic tissues. Pharmacological inhibition of FAT activity of p300 is associated with decreased collagen synthesis by fibroblasts in tissues and amelioration of organ fibrosis. Therefore, FAT-free p300 is superior for physiological tissue repair and must be exploited as a viable therapeutic target against multi-organ fibrosis. J. Cell. Biochem. 115: 1486-1489, 2014.

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KW - ORGAN FIBROSIS

KW - TISSUE REPAIR

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