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Thymosin β4 Deficiency Exacerbates Renal and Cardiac Injury in Angiotensin-II–Induced Hypertension

Nitin Kumar, Tang-Dong Liao, Cesar A. Romero, Mani Maheshwari, Edward L. Peterson and Oscar A. Carretero

Hypertension. 2018 Jun;71(6):1133-1142. doi: 10.1161/HYPERTENSIONAHA.118.10952. Epub 2018 Apr 9. PMID: 29632102

https://www.ncbi.nlm.nih.gov/pubmed/29632102

Nitin Kumar (USA)


1) Summarize your work in one sentence.

In this article, we investigated the role of endogenous peptide Thymosin beta 4, a G-actin binding peptide in Angiotensin-II induced renal and cardiac damage. 


2) Summarize your findings in one sentence.

We found that mice lacking thymosin beta 4 were more susceptible and sensitive to Angiotensin-II induced kidney and heart damage without affecting the blood-pressure. 


3) Which were the more important methods you used in this work? If it is not a traditional method you can briefly explain the concept of that methodology.

One of the important methods used was the echocardiography in mice, since it is technically challenging due to the small size of the heart and the high heart rate present in the mice. We also used traditional microscopy imaging and molecular techniques to evaluate kidney and heart damage.


4) What did you learn from this paper, what was your take-home message?

The most important concept of this paper other than the relevant role of the endogenous Thymosin beta 4 in cellular homeostasis, was the fact that the organ-damage was not only dependent on the blood- pressure (a mechanic effect), but also from other factors (such as loss of thymosin beta 4) that may increase the susceptibility to tissue damage, explaining some of the variability seen in target organ damage in patients.

 

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