Title: Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell
damage by inhibiting autophagy
Version: 8 Date: 16 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the study focuses on autophagy as a primary mechanism of VDR action, it could further
explore other potential molecular pathways involved in BA progression. For example, the role
of VDR in modulating inflammation or immune responses (e.g., via cytokines) is mentioned but
could be explored in more detail.
-The study focuses on poly(I:C)-induced damage, which mimics viral infection, but it would be
interesting to examine whether VDR activation offers protection against other forms of stress,
such as bacterial infections or bile acid-induced damage, which are also relevant to BA.
-While the RRV-induced BA mouse model is an appropriate choice for studying viral-induced
liver injury, it may not fully capture the complexity of BA, which is believed to be influenced by
both environmental and genetic factors. The inclusion of additional models or a more nuanced
discussion of model limitations could provide a more comprehensive view of VDR’s role in BA.
-Although in vitro experiments examine various doses of 1,25-VD3, it would be useful to include
a more detailed analysis of dose-response effects in clinical settings. The optimal dose and
duration of treatment for BA patients remain uncertain and would be important to clarify for
future clinical trials.
-The study focuses primarily on poly(I:C)-induced damage in BECs, which may not fully
replicate the diverse etiologies of BA, such as those caused by cytomegalovirus or environmental
toxins like biliatresone. More work is needed to extend these findings to other forms of BA.
Title: Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell
damage by inhibiting autophagy
Version: 8 Date: 16 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the study focuses on autophagy as a primary mechanism of VDR action, it could further
explore other potential molecular pathways involved in BA progression. For example, the role
of VDR in modulating inflammation or immune responses (e.g., via cytokines) is mentioned but
could be explored in more detail.
-The study focuses on poly(I:C)-induced damage, which mimics viral infection, but it would be
interesting to examine whether VDR activation offers protection against other forms of stress,
such as bacterial infections or bile acid-induced damage, which are also relevant to BA.
-While the RRV-induced BA mouse model is an appropriate choice for studying viral-induced
liver injury, it may not fully capture the complexity of BA, which is believed to be influenced by
both environmental and genetic factors. The inclusion of additional models or a more nuanced
discussion of model limitations could provide a more comprehensive view of VDR’s role in BA.
-Although in vitro experiments examine various doses of 1,25-VD3, it would be useful to include
a more detailed analysis of dose-response effects in clinical settings. The optimal dose and
duration of treatment for BA patients remain uncertain and would be important to clarify for
future clinical trials.
-The study focuses primarily on poly(I:C)-induced damage in BECs, which may not fully
replicate the diverse etiologies of BA, such as those caused by cytomegalovirus or environmental
toxins like biliatresone. More work is needed to extend these findings to other forms of BA.
Please review this paper.
user
Title: Vitamin D3/VDR alleviates double-stranded RNA virus -induced biliary epithelial cell
damage by inhibiting autophagy
Version: 8 Date: 16 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the study focuses on autophagy as a primary mechanism of VDR action, it could further
explore other potential molecular pathways involved in BA progression. For example, the role
of VDR in modulating inflammation or immune responses (e.g., via cytokines) is mentioned but
could be explored in more detail.
-The study focuses on poly(I:C)-induced damage, which mimics viral infection, but it would be
interesting to examine whether VDR activation offers protection against other forms of stress,
such as bacterial infections or bile acid-induced damage, which are also relevant to BA.
-While the RRV-induced BA mouse model is an appropriate choice for studying viral-induced
liver injury, it may not fully capture the complexity of BA, which is believed to be influenced by
both environmental and genetic factors. The inclusion of additional models or a more nuanced
discussion of model limitations could provide a more comprehensive view of VDR’s role in BA.
-Although in vitro experiments examine various doses of 1,25-VD3, it would be useful to include
a more detailed analysis of dose-response effects in clinical settings. The optimal dose and
duration of treatment for BA patients remain uncertain and would be important to clarify for
future clinical trials.
-The study focuses primarily on poly(I:C)-induced damage in BECs, which may not fully
replicate the diverse etiologies of BA, such as those caused by cytomegalovirus or environmental
toxins like biliatresone. More work is needed to extend these findings to other forms of BA.
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