?6?1Min et al., Endocrinology 2004
?6?1Nakai et al., J Dermatol Sci 2008
?6?1Rompe et al., Hypertension 2010
?6?1Steckelings et al., (Exp Dermatol 2004)
?6?1Yevdokimova et al., J Dermatol Sci 2007
?6?1Morihara et al., J Am Acad Dermatol 2006
?6?1Yahata et al., J Biol Chem 2006
?6?1Takeda et al., Am J Pathol 2004
并逐部分给予我的意见:Abstract:- In the case of AT1R-blockade, AT2R unmasking may indeed be important, but blockade of the AT1R thus interrupting AT1R-mediated actions of Ang II, is at least as important. The respective passage in the abstract is ambiguous.
Introduction:
- p.3, line 13: “disorders of RAS”: A “disorder” of the RAS has so far only been described for scleroderma (not saying whether the deregulated RAS is a primary cause or only a secondary phenomenon). It is indeed likely that the RAS is deregulated in the other mentioned dermatoses as well, but this is pure speculation and should be discussed as such.
- p.3, line 19: “existence of RAS in skin”: References 2 and 3 demonstrate only the existence of receptors, but not of the whole RAS in skin. Adequate references would be: Steckelings et al., Exp Dermatol or Philips MI et al., In: Saavedra J M, Timmermans P M W M, eds. Angiotensin receptors. New York: Plenum Press, 1994: 377–396.
- p.3, line 20: “It has been documented…”: It is correct that AT2R upregulation has been demonstrated in skin, and it is also correct that Ang II has been shown to accelerate cutaneous wound healing. However, it has never been shown that acceleration of wound healing by Ang II is mediated by the AT2R. In fact, this is rather unlikely, since the AT2R acts anti-proliferative.
- Chapter II 1: Physiological receptor expression should be addressed prior to receptor expression in pathology.
- p4, line 5 from bottom: “Ang II either…” Please add reference.
- chapter II 2: The high expression of Ang II receptors during foetal life indeed suggests a role in development. However, Ang II receptor knockout mice show no severe developmental deficits, in particular not in skin. Furthermore, there are almost no data about what specifically the role of the AT2R in development may be. This should be mentioned.
- chapter II 3: This chapter is much too short. For example, the description of deregulated receptor expression in some dermatoses by Takeda and Kondo (Am J Pathol 2001, Br J Dermatol 2001 and 2002) has not been cited. This chapter may further be the place for some speculations (based on data from non-cutaneous tissues) in which dermatoses the RAS may be disturbed.
- page 5, line 5: “Kawaguchi et al …in SSc fibroblasts, suggesting that… “: This is not a logical conclusion. What is the causal link between AT2R in SSc fibroblasts and excessive ECM production? Furthermore, expression of AT2R has been shown by several authors for normal fibroblasts.
- page 5, line 12: Steckelings is a woman (“her” colleagues).
- page 5, last section: The impact of AT2R expression on immune cells and of AT2R effects on vascularisation and neuroregeneration with regard to wound healing is not sufficiently discussed.
- p.6, 2 lines from bottom: “…restoring normality not only in the CV system but also in many tissues, such as skin.” Please provide a reference for the statement that the AT2R has been shown to restore normality in skin. 最后提交时杂志社会有一个勾选表 , 该文被我拒了该文编辑在结合另一个审稿人意见的情况下还是reject此文了 , 从投稿到最后给出decision约6个星期 , 应该说是正常速度了 。有意思的是中途 , 编辑发信催审稿了 , 估计是作者急着想知道结果 , 可以理解 , 想想之前的我们也何尝不是啊 , 每天都不停得刷屏 , 也写过催稿信 , 还以为没有用 , 甚至有时候也不“敢”写 , 因为害怕是否会有“反”作用 , 看来某些时候写信催催也还是可以的 。总之 , 审稿也未必是件好差事 , 不过倒是可以知己知彼 , 可以站在审稿人的角度去思考我们自己在写文章的时候应该注意什么 , 别人文章的有哪些优点、缺点 , 我们都可以好好去总结 , 同时我们也获得与最新研究领域的接触也为以后研究 , 能够写作提供更多的思路 。
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