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Pathophysiological role of different tubular epithelial cell death modes in acute kidney injury.

Sancho-Martínez SM, López-Novoa JM, López-Hernández FJ - Clin Kidney J (2015)

Bottom Line: Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens.For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant.Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Fisiología y Farmacología , Universidad de Salamanca , Salamanca , Spain ; Instituto de Investigación Biomédica de Salamanca (IBSAL) , Salamanca , Spain ; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo , Madrid , Spain.

ABSTRACT
The histological substrate of many forms of intrinsic acute kidney injury (AKI) has been classically attributed to tubular necrosis. However, more recent studies indicate that necrosis is not the main form of cell death in AKI and that other forms such as apoptosis, regulated necrosis (i.e. necroptosis and parthanatos), autophagic cell death and mitotic catastrophe, also participate in AKI and that their contribution depends on the cause and stage of AKI. Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens. We also discuss the pathophysiological mechanisms linking tubule epithelial cell death with reduced glomerular filtration, azotaemia and hydroelectrolytic imbalance. For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant. Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

No MeSH data available.


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Schematic representation of the main signalling pathways of different cell death modes, and the pathophysiological mechanisms activated by cell death modes in acute kidney injury.
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SFV069F1: Schematic representation of the main signalling pathways of different cell death modes, and the pathophysiological mechanisms activated by cell death modes in acute kidney injury.

Mentions: Since the first descriptions of programmed cell death mechanisms in the mid-1960s, many attempts have been made to classify cell death forms and their physiological and pathological consequences. The first classifications of cell death were based on the morphological characteristics of the dying cells. When biochemical pathways and genes involved in cell death started to be described, the classification of cell death types was based also on biochemical and molecular criteria (Table 2 and Figure 1). Because there are many classifications of cell death relying on different criteria, we have chosen to use in the present review the last published recommendations of The Nomenclature Committee on Cell Death (NCCD) [12]. This classification applies to both in vitro and in vivo settings and includes apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe, as well as some other types of cell death such as anoikis, entosis, NETosis, parthanatos, ferroptosis, and pyroptosis (Table 2 and Figure 1).Table 2.


Pathophysiological role of different tubular epithelial cell death modes in acute kidney injury.

Sancho-Martínez SM, López-Novoa JM, López-Hernández FJ - Clin Kidney J (2015)

Schematic representation of the main signalling pathways of different cell death modes, and the pathophysiological mechanisms activated by cell death modes in acute kidney injury.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581387&req=5

SFV069F1: Schematic representation of the main signalling pathways of different cell death modes, and the pathophysiological mechanisms activated by cell death modes in acute kidney injury.
Mentions: Since the first descriptions of programmed cell death mechanisms in the mid-1960s, many attempts have been made to classify cell death forms and their physiological and pathological consequences. The first classifications of cell death were based on the morphological characteristics of the dying cells. When biochemical pathways and genes involved in cell death started to be described, the classification of cell death types was based also on biochemical and molecular criteria (Table 2 and Figure 1). Because there are many classifications of cell death relying on different criteria, we have chosen to use in the present review the last published recommendations of The Nomenclature Committee on Cell Death (NCCD) [12]. This classification applies to both in vitro and in vivo settings and includes apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe, as well as some other types of cell death such as anoikis, entosis, NETosis, parthanatos, ferroptosis, and pyroptosis (Table 2 and Figure 1).Table 2.

Bottom Line: Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens.For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant.Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Fisiología y Farmacología , Universidad de Salamanca , Salamanca , Spain ; Instituto de Investigación Biomédica de Salamanca (IBSAL) , Salamanca , Spain ; Instituto Reina Sofía de Investigación Nefrológica, Fundación Iñigo Álvarez de Toledo , Madrid , Spain.

ABSTRACT
The histological substrate of many forms of intrinsic acute kidney injury (AKI) has been classically attributed to tubular necrosis. However, more recent studies indicate that necrosis is not the main form of cell death in AKI and that other forms such as apoptosis, regulated necrosis (i.e. necroptosis and parthanatos), autophagic cell death and mitotic catastrophe, also participate in AKI and that their contribution depends on the cause and stage of AKI. Herein, we briefly summarize the main characteristics of the major types of cell death and we also critically review the existing evidence on the occurrence of different types of cell death reported in the most common experimental models of AKI and human specimens. We also discuss the pathophysiological mechanisms linking tubule epithelial cell death with reduced glomerular filtration, azotaemia and hydroelectrolytic imbalance. For instance, special relevance is given to the analysis of the inflammatory component of some forms of cell death over that of others, as an important and differential pathophysiological determinant. Finally, known molecular mechanisms and signalling pathways involved in each cell death type pose appropriate targets to specifically prevent or reverse AKI, provided that further knowledge of their participation and repercussion in each AKI syndrome is progressively increased in the near future.

No MeSH data available.


Related in: MedlinePlus