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Volume 45
Issue 3
10.3390/cimb45030141
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Review
Peer-Review Record

Advances in Ion Channel, Non-Desmosomal Variants and Autophagic Mechanisms Implicated in Arrhythmogenic Cardiomyopathy

Curr. Issues Mol. Biol. 2023, 45(3), 2186-2200; https://doi.org/10.3390/cimb45030141
by Kexin Li 1,2,†, Yufeng Jiang 1,2,†, Yiyao Zeng 1,2 and Yafeng Zhou 1,2,*
Reviewer 1: Anonymous
Reviewer 2:
Narcis Tribulova
Curr. Issues Mol. Biol. 2023, 45(3), 2186-2200; https://doi.org/10.3390/cimb45030141
Submission received: 9 February 2023 / Revised: 28 February 2023 / Accepted: 1 March 2023 / Published: 7 March 2023
(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

Round 1

Reviewer 1 Report

Although it is a well designed and well written article, I would like to point out some deficiencies:

1- There should be a separate section on the genetic origin of arrhythmogenic cardiomyopathy.

2- There should be a table of the main studies on arrhythmogenic cardiomyopathy.

3-There should be more information about premature beats in the discussion section. For example: You can use 'Ambulatory blood pressure outcomes and heart rate variability in patients with premature ventricular contractions Clinical and Experimental Hypertension 2018 40 (3), 251-256.' titled study.

4-You need more comprehensive discussion part and your own results.

 

 

 

 

 

 

Author Response

Please see the attachment.

Author Response File: Author Response.docx

Reviewer 2 Report

Manuscript refers to arrhythmogenic cardiomyopathy that is a genetic cardiomyopathy of the heart muscle (myocardium) due to its replacement by both scar (fibrosis) and fat. This can affect the right ventricle, the left ventricle, or both cardiac ventricles. Such changes profoundly affect electrical and mechanical properties of the heart resulting in the occurrence of malignant arrhythmias and heart failure. Authors reviewed a recent studies focused on involvement ion channels, autophagy and non-desmosomal variants in the development of this cardiomyopathy that may improve its diagnostic and treatment.

 

In general, if paper should be informative for readers, it would be appreciated to avoid long paragraphs.

There are more publications regarding to connexin43 and connexin-interacting proteins (desmoglein, desmoplakin, plakophillin-2, etc) alterations in arrhythmogenic cardiomyopathy, while missing in the manuscript.

Figure schematically illustrating these factors implicated in ACM will be appreciated.

Terminology of ion channel channels in subheadings should be unified.

Figure 1 and 2 are authors artwork or from the paper that should be cited?

The Table of novel ACM genes would be appreciated.

The chapter of Perspectives or future research should be included.

Author Response

Please see the attachment.

Author Response File: Author Response.docx

Round 2

Reviewer 1 Report

No comments.

Reviewer 2 Report

Revised version of the review article is improved, thereby more interesting for readers.

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