Is what autophagy protective?
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Autophagy plays a protective role in various contexts. In cancer, autophagy has a cytoprotective mechanism that helps overcome resistance to cancer therapies, making it a potential target for cancer treatment . In age-related macular degeneration (AMD), selective autophagy in the retina protects against retinal degeneration and preserves vision . In hepatic ischemia/reperfusion (I/R) injury, autophagy can both promote cell survival and protect against autophagic cell death, depending on the circumstances . Autophagy also has a protective effect in cerebral damage caused by different models, inhibiting the inflammatory response and reducing injury . The nature of autophagy induced by topoisomerase I inhibitors is not clearly defined, but targeting autophagy may have potential as a therapeutic strategy to enhance the antitumor response and overcome drug resistance .
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| Papers (5) | Insight |
|---|---|
1 Citations | The paper does not clearly define whether autophagy induced by topoisomerase I inhibitors is cytotoxic, cytoprotective, or non-protective. |
Open access•Journal Article 10 Citations | Autophagy is protective against cerebral ischemic reperfusion injury by inhibiting neuroinflammation, as stated in the paper. |
15 Citations | The paper discusses how autophagy regulation can protect against liver injury induced by ischaemia/reperfusion in liver surgery. |
| The paper does not explicitly mention whether autophagy is protective. | |
| Selective autophagy is protective in the retina and can be utilized to preserve vision in both physiological and pathological conditions. |
Related Questions
How does an increase in autophagy inhibit phagocytosis?4 answersAn increase in autophagy can inhibit phagocytosis through several interconnected mechanisms, as evidenced by recent research findings. Autophagy, a cellular process for degrading and recycling cellular components, has been shown to have a complex relationship with phagocytosis, the process by which cells engulf and digest external particles, including pathogens.
One mechanism involves the modulation of autophagy-related genes and proteins, which can directly impact the phagocytic ability of macrophages. For instance, the inhibition of autophagy through 3-MA led to an increase in the phagocytic ability of macrophages against MRSA, suggesting that active autophagy can suppress this ability. Similarly, the knockdown of GMFg, a regulator of autophagy, resulted in increased phagocytic activity, indicating that autophagy can negatively regulate phagocytosis.
Furthermore, autophagy dysfunction, induced by factors such as fine particulate matter (FPM), impairs the phagocytic function of macrophages, highlighting the delicate balance between autophagy and phagocytosis necessary for optimal cellular function. In the context of bacterial infection, autophagy has been shown to promote the clearance of pathogens like Treponema pallidum by macrophages, suggesting that while autophagy can inhibit phagocytosis, it can also facilitate the clearance of certain pathogens.
Cigarette smoke exposure, which impairs autophagy, also leads to diminished bacterial clearance via phagocytosis, further illustrating the negative impact of disrupted autophagy on phagocytosis. Non-canonical autophagy pathways, such as those involving V-ATPase, also play a role in modulating phagocytosis, indicating a broader regulatory mechanism. Additionally, in stroke models, microglial phagocytosis dysfunction was not directly linked to transcriptional changes but to energy depletion and autophagy induction, suggesting that autophagy can indirectly affect phagocytosis through energy management. Lastly, pathogens have evolved mechanisms to manipulate host autophagy to evade phagocytosis, further complicating the relationship between these two processes.
In summary, an increase in autophagy can inhibit phagocytosis through the modulation of autophagy-related genes and proteins, the impairment of cellular functions by external factors, and the manipulation by pathogens to evade immune responses. This intricate relationship underscores the need for a balanced autophagic activity to maintain effective phagocytic function.
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