On 2015 Aug 10, NephJC - Nephrology Journal Club commented:

This study was discussed on July 28 and 29th 2015 in the open online nephrology journal club, #NephJC, on twitter .

Introductory explanatory comments, written by Matt Sparks, are available at the NephJC.

There was a very lively discussion, which included about 50 participants, enriched by the active engagement by two of the authors, Ben Humphreys and Rafael Kramann, and was complete with many citations to related research articles.

A transcript and a curated (i.e. Storified) version of the tweetchat are available from the NephJC website.

The highlights of the tweetchat discussion were:

• The study does help establish that Gli1+ perivascular ('pericytes') MSC-like cells are the source of ~70% of myofibroblasts after organ injury, and are key players in the subsequent fibrosis.

• Successful/effective targeting of this pathway leads to less fibrosis in preservation of heart function after transverse aortic banding (a heart failure model), however substantial hurdles still exist in terms of delivering a potential therapeutic intervention to lessen fibrosis but ensuring the protective effects of fibrosis are not inhibited.

• The authors' did remarkable work in leveraging elegant techniques such as lineage tracing, multiple organ injury models, parabiosis and diphtheria toxin/Gli1 knockout.

Interested individuals can track and join in the conversation by following @NephJC or #NephJC, or visit the webpage at NephJC.com.

On 2015 Aug 10, NephJC - Nephrology Journal Club commented:

This study was discussed on July 28 and 29th 2015 in the open online nephrology journal club, #NephJC, on twitter .

Introductory explanatory comments, written by Matt Sparks, are available at the NephJC.

There was a very lively discussion, which included about 50 participants, enriched by the active engagement by two of the authors, Ben Humphreys and Rafael Kramann, and was complete with many citations to related research articles.

A transcript and a curated (i.e. Storified) version of the tweetchat are available from the NephJC website.

The highlights of the tweetchat discussion were:

• The study does help establish that Gli1+ perivascular ('pericytes') MSC-like cells are the source of ~70% of myofibroblasts after organ injury, and are key players in the subsequent fibrosis.

• Successful/effective targeting of this pathway leads to less fibrosis in preservation of heart function after transverse aortic banding (a heart failure model), however substantial hurdles still exist in terms of delivering a potential therapeutic intervention to lessen fibrosis but ensuring the protective effects of fibrosis are not inhibited.

• The authors' did remarkable work in leveraging elegant techniques such as lineage tracing, multiple organ injury models, parabiosis and diphtheria toxin/Gli1 knockout.

Interested individuals can track and join in the conversation by following @NephJC or #NephJC, or visit the webpage at NephJC.com.