Effect of Transcriptional Regulatory Factors and Signal Transduction on Cell Regeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 9009

Special Issue Editor


E-Mail Website
Guest Editor
Institute of Cell Biology, Biocenter, Medical University of Innsbruck, Innrain 80-82, 6020 Innsbruck, Austria
Interests: transcriptional regulation; differentiation; regeneration; cell signaling

Special Issue Information

Dear Colleagues,

Cellular regeneration, differentiation, and re-differentiation represent terms from basic research that have found application in therapeutics. In addition to many other attractive areas, a comprehensive discussion on myocardial cell regeneration has initiated cardiac cell therapy, involving interventions that optimize muscle cell regeneration, which is important for muscle injury repair, and cochlear sensory epithelium hair cell regeneration, which provides a therapeutic approach to recover hearing sensitivity.

Tissue regeneration studies focus on processes by which an injured organ regrows to offset the missed cells. This field has been at the focus of intense research because it represents the cornerstone of tissue engineering, the creation of artificial organs, and the generation of therapeutic stem cells for different types of mature cells. Efforts are dedicated to understanding organ regeneration, its molecular basis, signaling pathways, and the regulatory molecules required to procure a complete restoration.

In humans, limitations on the regenerative capacity of specific tissues and organs make it difficult to recover from diseases. The ultimate goal of cell and tissue regeneration is understanding the control of these events. Therefore, it is important to identify processes involved in the regulation of cell remodeling after cell damage to provide helpful information for challenging diseases.

The focus of the present Special Issue is on advances in cellular biology of regeneration, mechanisms and molecules involved in processes of repair, and the recovery of functionality after tissue damage. An ambitious goal is to provide ideas for future therapeutic approaches based on the current newest findings.

Dr. Ilja Vietor
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • adult stem cells
  • stem cell therapy
  • tissue
  • physiological and reparative regeneration
  • signaling pathways
  • gene expression
  • cellular differentiation
  • transdifferentiation
  • autophagy

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

16 pages, 6578 KiB  
Article
Effect of Hypoxia in the Transcriptomic Profile of Lung Fibroblasts from Idiopathic Pulmonary Fibrosis
by Yair Romero, Yalbi Itzel Balderas-Martínez, Miguel Angel Vargas-Morales, Manuel Castillejos-López, Joel Armando Vázquez-Pérez, Jazmín Calyeca, Luz María Torres-Espíndola, Nelly Patiño, Angel Camarena, Ángeles Carlos-Reyes, Edgar Flores-Soto, Guadalupe León-Reyes, Martha Patricia Sierra-Vargas, Iliana Herrera, Erika Rubí Luis-García, Víctor Ruiz, Rafael Velázquez-Cruz and Arnoldo Aquino-Gálvez
Cells 2022, 11(19), 3014; https://doi.org/10.3390/cells11193014 - 27 Sep 2022
Cited by 2 | Viewed by 2397
Abstract
Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by exacerbated extracellular matrix deposition that disrupts oxygen exchange. Hypoxia and its transcription factors (HIF-1α and 2α) influence numerous circuits that could perpetuate fibrosis by increasing myofibroblasts differentiation and by promoting extracellular matrix accumulation. [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by exacerbated extracellular matrix deposition that disrupts oxygen exchange. Hypoxia and its transcription factors (HIF-1α and 2α) influence numerous circuits that could perpetuate fibrosis by increasing myofibroblasts differentiation and by promoting extracellular matrix accumulation. Therefore, this work aimed to elucidate the signature of hypoxia in the transcriptomic circuitry of IPF-derived fibroblasts. To determine this transcriptomic signature, a gene expression analysis with six lines of lung fibroblasts under normoxia or hypoxia was performed: three cell lines were derived from patients with IPF, and three were from healthy donors, a total of 36 replicates. We used the Clariom D platform, which allows us to evaluate a huge number of transcripts, to analyze the response to hypoxia in both controls and IPF. The control′s response is greater by the number of genes and complexity. In the search for specific genes responsible for the IPF fibroblast phenotype, nineteen dysregulated genes were found in lung fibroblasts from IPF patients in hypoxia (nine upregulated and ten downregulated). In this sense, the signaling pathways revealed to be affected in the pulmonary fibroblasts of patients with IPF may represent an adaptation to chronic hypoxia. Full article
Show Figures

Figure 1

Review

Jump to: Research

18 pages, 1999 KiB  
Review
Functional Repercussions of Hypoxia-Inducible Factor-2α in Idiopathic Pulmonary Fibrosis
by Ana Karen Torres-Soria, Yair Romero, Yalbi I. Balderas-Martínez, Rafael Velázquez-Cruz, Luz Maria Torres-Espíndola, Angel Camarena, Edgar Flores-Soto, Héctor Solís-Chagoyán, Víctor Ruiz, Ángeles Carlos-Reyes, Citlaltepetl Salinas-Lara, Erika Rubí Luis-García, Jaime Chávez, Manuel Castillejos-López and Arnoldo Aquino-Gálvez
Cells 2022, 11(19), 2938; https://doi.org/10.3390/cells11192938 - 20 Sep 2022
Cited by 1 | Viewed by 2846
Abstract
Hypoxia and hypoxia-inducible factors (HIFs) are essential in regulating several cellular processes, such as survival, differentiation, and the cell cycle; this adaptation is orchestrated in a complex way. In this review, we focused on the impact of hypoxia in the physiopathology of idiopathic [...] Read more.
Hypoxia and hypoxia-inducible factors (HIFs) are essential in regulating several cellular processes, such as survival, differentiation, and the cell cycle; this adaptation is orchestrated in a complex way. In this review, we focused on the impact of hypoxia in the physiopathology of idiopathic pulmonary fibrosis (IPF) related to lung development, regeneration, and repair. There is robust evidence that the responses of HIF-1α and -2α differ; HIF-1α participates mainly in the acute phase of the response to hypoxia, and HIF-2α in the chronic phase. The analysis of their structure and of different studies showed a high specificity according to the tissue and the process involved. We propose that hypoxia-inducible transcription factor 2a (HIF-2α) is part of the persistent aberrant regeneration associated with developing IPF. Full article
Show Figures

Graphical abstract

17 pages, 2255 KiB  
Review
Signal Transduction Regulators in Axonal Regeneration
by Barbara Hausott, Rudolf Glueckert, Anneliese Schrott-Fischer and Lars Klimaschewski
Cells 2022, 11(9), 1537; https://doi.org/10.3390/cells11091537 - 4 May 2022
Cited by 4 | Viewed by 3220
Abstract
Intracellular signal transduction in response to growth factor receptor activation is a fundamental process during the regeneration of the nervous system. In this context, intracellular inhibitors of neuronal growth factor signaling have become of great interest in the recent years. Among them are [...] Read more.
Intracellular signal transduction in response to growth factor receptor activation is a fundamental process during the regeneration of the nervous system. In this context, intracellular inhibitors of neuronal growth factor signaling have become of great interest in the recent years. Among them are the prominent signal transduction regulators Sprouty (SPRY) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN), which interfere with major signaling pathways such as extracellular signal-regulated kinase (ERK) or phosphoinositide 3-kinase (PI3K)/Akt in neurons and glial cells. Furthermore, SPRY and PTEN are themselves tightly regulated by ubiquitin ligases such as c-casitas b-lineage lymphoma (c-CBL) or neural precursor cell expressed developmentally down-regulated protein 4 (NEDD4) and by different microRNAs (miRs) including miR-21 and miR-222. SPRY, PTEN and their intracellular regulators play an important role in the developing and the lesioned adult central and peripheral nervous system. This review will focus on the effects of SPRY and PTEN as well as their regulators in various experimental models of axonal regeneration in vitro and in vivo. Targeting these signal transduction regulators in the nervous system holds great promise for the treatment of neurological injuries in the future. Full article
Show Figures

Figure 1

Back to TopTop