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Molecular Mechanisms of Cell Death in Epithelial Cells: The Role of p53 Family

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3569

Special Issue Editor


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Guest Editor
Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Research Council, CNR, 70126 Bari, Italy
Interests: p53; cancers; tumor suppression; chemotherapy; transcriptomics; genomics; p53 gene family; transcriptional regulation; next-generation sequencing
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Special Issue Information

Dear Colleagues, 

P53 represents a key transcriptional factor involved in cellular response to genotoxic stresses. Cell death is the main p53-dependent cellular response to severe stress and irreparable DNA damage. All of the organism tissues and organs may suffer from stress coming from several sources, and epithelial tissue represents the first defense barrier to solar rays, hazardous substances and other potential dangerous sources of DNA damaging agents. In these terms, it is important to know the role of p53 (and of its related proteins family p63 and p73) in defending organisms from DNA-damaged dependent diseases onset, such as cancer. It is likewise important to know the consequences of a functional inactivation of the physiological activities of the proteins involved in cellular homeostasis and defense from genotoxic stresses, by analyzing the molecular alteration both in p53 family protein expression and in the downstream pathways involved in mechanisms such as cell cycle arrest, DNA repair, and cell death, above all. This Special Issue aims at collecting and shedding light on all the latest research and discoveries in this field, in order to give useful information for diagnostical knowledge as well as for pharmaceutical and therapeutical applications by the synthesis of molecular drugs.

Dr. Mariano Francesco Caratozzolo
Guest Editor

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Keywords

  • P53

  • tumor suppression
  • apoptosis
  • DNA damage
  • genotoxic stress
  • molecular network
  • P53 gene family
  • epithelial homeostasis
  • P63 and p73

Published Papers (1 paper)

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Review

29 pages, 1509 KiB  
Review
p53 and Myofibroblast Apoptosis in Organ Fibrosis
by Kealan McElhinney, Mustapha Irnaten and Colm O’Brien
Int. J. Mol. Sci. 2023, 24(7), 6737; https://doi.org/10.3390/ijms24076737 - 4 Apr 2023
Cited by 5 | Viewed by 3245
Abstract
Organ fibrosis represents a dysregulated, maladaptive wound repair response that results in progressive disruption of normal tissue architecture leading to detrimental deterioration in physiological function, and significant morbidity/mortality. Fibrosis is thought to contribute to nearly 50% of all deaths in the Western world [...] Read more.
Organ fibrosis represents a dysregulated, maladaptive wound repair response that results in progressive disruption of normal tissue architecture leading to detrimental deterioration in physiological function, and significant morbidity/mortality. Fibrosis is thought to contribute to nearly 50% of all deaths in the Western world with current treatment modalities effective in slowing disease progression but not effective in restoring organ function or reversing fibrotic changes. When physiological wound repair is complete, myofibroblasts are programmed to undergo cell death and self-clearance, however, in fibrosis there is a characteristic absence of myofibroblast apoptosis. It has been shown that in fibrosis, myofibroblasts adopt an apoptotic-resistant, highly proliferative phenotype leading to persistent myofibroblast activation and perpetuation of the fibrotic disease process. Recently, this pathological adaptation has been linked to dysregulated expression of tumour suppressor gene p53. In this review, we discuss p53 dysregulation and apoptotic failure in myofibroblasts and demonstrate its consistent link to fibrotic disease development in all types of organ fibrosis. An enhanced understanding of the role of p53 dysregulation and myofibroblast apoptosis may aid in future novel therapeutic and/or diagnostic strategies in organ fibrosis. Full article
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