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Modulation of inflammation by autophagy: Consequences for human disease

View Article: PubMed Central - PubMed

ABSTRACT

Autophagy and inflammation are 2 fundamental biological processes involved in both physiological and pathological conditions. Through its crucial role in maintaining cellular homeostasis, autophagy is involved in modulation of cell metabolism, cell survival, and host defense. Defective autophagy is associated with pathological conditions such as cancer, autoimmune disease, neurodegenerative disease, and senescence. Inflammation represents a crucial line of defense against microorganisms and other pathogens, and there is increasing evidence that autophagy has important effects on the induction and modulation of the inflammatory reaction; understanding the balance between these 2 processes may point to important possibilities for therapeutic targeting. This review focuses on the crosstalk between autophagy and inflammation as an emerging field with major implications for understanding the host defense on the one hand, and for the pathogenesis and treatment of immune-mediated diseases on the other hand.

No MeSH data available.


Related in: MedlinePlus

The role of crosstalk between autophagy and inflammation in cancer. Induction of autophagy is a double-edged sword with both protumorigenic and antitumorigenic effects. Processes downstream of autophagy that influence tumor progression and treatment resistance are comprised of cell survival pathways and recruitment of innate immune cells following release of DAMPs by necrotic tumor cells. Conversely, antitumorigenic signaling is evoked by autophagy-mediated immunogenic cell death and inhibition of tumor-associated inflammation. An outstanding example of the diverse and apparently opposite effects of autophagy on cancer initiation and progression is the induction of cellular senescence and subsequent removal of senescent cells; depending on the cellular context this is either pro- or anti-tumorigenic. APC, antigen-presenting cell.
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f0004: The role of crosstalk between autophagy and inflammation in cancer. Induction of autophagy is a double-edged sword with both protumorigenic and antitumorigenic effects. Processes downstream of autophagy that influence tumor progression and treatment resistance are comprised of cell survival pathways and recruitment of innate immune cells following release of DAMPs by necrotic tumor cells. Conversely, antitumorigenic signaling is evoked by autophagy-mediated immunogenic cell death and inhibition of tumor-associated inflammation. An outstanding example of the diverse and apparently opposite effects of autophagy on cancer initiation and progression is the induction of cellular senescence and subsequent removal of senescent cells; depending on the cellular context this is either pro- or anti-tumorigenic. APC, antigen-presenting cell.

Mentions: The relationship between inflammation and cancer has long been recognized. Many chronic inflammatory conditions, such as inflammatory bowel disease, chronic hepatitis, or pancreatitis are clearly recognized as precursors of malignancies in the respective organs.174-177 Moreover, the immune system is the most important defense mechanism that identifies and eliminates malignant transformed cells and prevents tumor progression and metastasis. Autophagy has a modulatory role that shapes the interface between cancer and immune response, including effects on both tumor cells and immune cells, which subsequently influence the survival and function of, and interplay between, these cells and ultimately results in either tumor-promoting or tumor-suppressing effects (Fig. 4).Figure 4.


Modulation of inflammation by autophagy: Consequences for human disease
The role of crosstalk between autophagy and inflammation in cancer. Induction of autophagy is a double-edged sword with both protumorigenic and antitumorigenic effects. Processes downstream of autophagy that influence tumor progression and treatment resistance are comprised of cell survival pathways and recruitment of innate immune cells following release of DAMPs by necrotic tumor cells. Conversely, antitumorigenic signaling is evoked by autophagy-mediated immunogenic cell death and inhibition of tumor-associated inflammation. An outstanding example of the diverse and apparently opposite effects of autophagy on cancer initiation and progression is the induction of cellular senescence and subsequent removal of senescent cells; depending on the cellular context this is either pro- or anti-tumorigenic. APC, antigen-presenting cell.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836004&req=5

f0004: The role of crosstalk between autophagy and inflammation in cancer. Induction of autophagy is a double-edged sword with both protumorigenic and antitumorigenic effects. Processes downstream of autophagy that influence tumor progression and treatment resistance are comprised of cell survival pathways and recruitment of innate immune cells following release of DAMPs by necrotic tumor cells. Conversely, antitumorigenic signaling is evoked by autophagy-mediated immunogenic cell death and inhibition of tumor-associated inflammation. An outstanding example of the diverse and apparently opposite effects of autophagy on cancer initiation and progression is the induction of cellular senescence and subsequent removal of senescent cells; depending on the cellular context this is either pro- or anti-tumorigenic. APC, antigen-presenting cell.
Mentions: The relationship between inflammation and cancer has long been recognized. Many chronic inflammatory conditions, such as inflammatory bowel disease, chronic hepatitis, or pancreatitis are clearly recognized as precursors of malignancies in the respective organs.174-177 Moreover, the immune system is the most important defense mechanism that identifies and eliminates malignant transformed cells and prevents tumor progression and metastasis. Autophagy has a modulatory role that shapes the interface between cancer and immune response, including effects on both tumor cells and immune cells, which subsequently influence the survival and function of, and interplay between, these cells and ultimately results in either tumor-promoting or tumor-suppressing effects (Fig. 4).Figure 4.

View Article: PubMed Central - PubMed

ABSTRACT

Autophagy and inflammation are 2 fundamental biological processes involved in both physiological and pathological conditions. Through its crucial role in maintaining cellular homeostasis, autophagy is involved in modulation of cell metabolism, cell survival, and host defense. Defective autophagy is associated with pathological conditions such as cancer, autoimmune disease, neurodegenerative disease, and senescence. Inflammation represents a crucial line of defense against microorganisms and other pathogens, and there is increasing evidence that autophagy has important effects on the induction and modulation of the inflammatory reaction; understanding the balance between these 2 processes may point to important possibilities for therapeutic targeting. This review focuses on the crosstalk between autophagy and inflammation as an emerging field with major implications for understanding the host defense on the one hand, and for the pathogenesis and treatment of immune-mediated diseases on the other hand.

No MeSH data available.


Related in: MedlinePlus