Autophagy, apoptosis, ferroptosis, and necroptosis play a key role in human diseases including, cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease among others. Promising therapeutic drugs which induce or inhibit autophagy, apoptosis, ferroptosis, and necroptosis, have been reported to abrogate tumor development and growth, as well as other diseases. For a more comprehensive understanding and clarification of these cells’ fate-related molecular mechanism in diseases, further studies in autophagy, apoptosis, ferroptosis, and necroptosis are critical.
Autophagy, apoptosis, ferroptosis, and necroptosis not only play an important role in physiological, but also pathological processes. Therefore it is not a surprise that they are closely related to many human diseases including cancer, aging, and neurodegenerative diseases. These processes have become the emerging biomarker or targets in human diseases. The main purpose of this topic is to identify and screen more potential molecular biomarkers and targets in autophagy, apoptosis, ferroptosis, and necroptosis. Furthermore, we aim to clarify the therapeutic effects related to molecular mechanisms. Through experimental analysis, we can provide valuable biomarkers and a feasible treatment scheme for dysfunctional cell fate-related human diseases. Therefore, we encourage authors to submit original scientific research achievements and the latest research progress highlighting this area of research.
The Research Topic welcomes articles covering, but not limited to, the following topics:
-Screening drugs or compounds and efficacy evaluation of compounds in all experimental systems (cancer, aging, neurodegenerative diseases, etc.) by inducing or inhibiting autophagy, apoptosis, ferroptosis, and necroptosis;
-The molecular mechanism of compounds in treating human diseases through autophagy, apoptosis, ferroptosis, and necroptosis.
We welcome manuscripts, such as original research (basic science, translational), and review articles (both comprehensive overviews and mini-reviews).
Autophagy, apoptosis, ferroptosis, and necroptosis play a key role in human diseases including, cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease among others. Promising therapeutic drugs which induce or inhibit autophagy, apoptosis, ferroptosis, and necroptosis, have been reported to abrogate tumor development and growth, as well as other diseases. For a more comprehensive understanding and clarification of these cells’ fate-related molecular mechanism in diseases, further studies in autophagy, apoptosis, ferroptosis, and necroptosis are critical.
Autophagy, apoptosis, ferroptosis, and necroptosis not only play an important role in physiological, but also pathological processes. Therefore it is not a surprise that they are closely related to many human diseases including cancer, aging, and neurodegenerative diseases. These processes have become the emerging biomarker or targets in human diseases. The main purpose of this topic is to identify and screen more potential molecular biomarkers and targets in autophagy, apoptosis, ferroptosis, and necroptosis. Furthermore, we aim to clarify the therapeutic effects related to molecular mechanisms. Through experimental analysis, we can provide valuable biomarkers and a feasible treatment scheme for dysfunctional cell fate-related human diseases. Therefore, we encourage authors to submit original scientific research achievements and the latest research progress highlighting this area of research.
The Research Topic welcomes articles covering, but not limited to, the following topics:
-Screening drugs or compounds and efficacy evaluation of compounds in all experimental systems (cancer, aging, neurodegenerative diseases, etc.) by inducing or inhibiting autophagy, apoptosis, ferroptosis, and necroptosis;
-The molecular mechanism of compounds in treating human diseases through autophagy, apoptosis, ferroptosis, and necroptosis.
We welcome manuscripts, such as original research (basic science, translational), and review articles (both comprehensive overviews and mini-reviews).