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Exploring the origin and limitations of kidney regeneration
Author(s) -
Endo Tomomi,
Nakamura Jin,
Sato Yuki,
Asada Misako,
Yamada Ryo,
Takase Masayuki,
Takaori Koji,
Oguchi Akiko,
Iguchi Taku,
Higashi Atsuko Y,
Ohbayashi Tetsuya,
Nakamura Tomoyuki,
Muso Eri,
Kimura Takeshi,
Yanagita Motoko
Publication year - 2015
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.4514
Subject(s) - regeneration (biology) , kidney , biology , microbiology and biotechnology , endocrinology
Epidemiological findings indicate that acute kidney injury ( AKI ) increases the risk for chronic kidney disease ( CKD ), although the molecular mechanism remains unclear. Genetic fate mapping demonstrated that nephrons, functional units in the kidney, are repaired by surviving nephrons after AKI . However, the cell population that repairs damaged nephrons and their repair capacity limitations remain controversial. To answer these questions, we generated a new transgenic mouse strain in which mature proximal tubules, the segment predominantly damaged during AKI , could be genetically labelled at desired time points. Using this strain, massive proliferation of mature proximal tubules is observed during repair, with no dilution of the genetic label after the repair process, demonstrating that proximal tubules are repaired mainly by their own proliferation. Furthermore, acute tubular injury caused significant shortening of proximal tubules associated with interstitial fibrosis, suggesting that proximal tubules have a limited capacity to repair. Understanding the mechanism of this limitation might clarify the mechanism of the AKI ‐to‐ CKD continuum. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.