Is autophagy protective?
Best insight from top research papers
Autophagy has been shown to have a protective role in various contexts. It helps maintain intracellular homeostasis by eliminating damaged or unnecessary proteins and organelles . In the context of cancer, autophagy has a dual role, with both cytoprotective and cytotoxic effects. It can promote resistance to cancer therapies, but selective autophagy inhibitors have been developed to overcome this resistance . Autophagy has also been found to have a neuroprotective effect, as seen in a study where autophagy regulation through the Akt/mTOR pathway protected neurons from oxygen-glucose deprivation/re-oxygenation-induced damage . In the case of alcoholic liver disease, autophagy activation has been shown to alleviate liver damage by restoring lysosome function . Overall, autophagy plays a protective role in various contexts, but its effects can vary depending on the specific disease or condition being studied.
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| Papers (5) | Insight |
|---|---|
1 Citations | The paper does not directly state whether autophagy is protective. |
| Yes, selective autophagy plays a protective role in the retina and can be used to preserve vision in physiological or pathological conditions. | |
1 Citations | The paper does not clearly define whether autophagy induced by topoisomerase I inhibitors is cytotoxic, cytoprotective, or non-protective. |
| The paper states that autophagy activation plays a dual role during cerebral ischemic injury. Moderate autophagy promotes neuroprotection, while chronic excessive autophagy can lead to neuron death and tissue damage. Therefore, autophagy can be protective under certain conditions. | |
| The paper states that autophagy has a cytoprotective mechanism and is associated with overcoming resistance to cancer therapies. |
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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