Abstract：
:Several hypotheses have been developed to interpret the progression of tubulointerstitial fibrosis (TF), including senescence, epithelial-mesenchymal transition, inflammation, chronic hypoxia, and reactive oxygen species. All of these hypotheses are based on persistent cell injury and localized cell death. Proliferation of neighboring renal tubular epithelial cells (RTECs) is beneficial for organ function recovery from acute injury. However, compensatory proliferation is not always advantageous, as the proliferating cells are vulnerable to ongoing detrimental stimuli, such as inflammation, endocrine stress, high blood pressure, hypoxia/ischemia, and the like. Cell injury and death promotes secretion of growth factors, which evokes proliferation of RTECs; entering the cell cycle makes the RTECs more vulnerable to injury and death. Under persistent stress, death and proliferation are mutually promoted and form the vicious circle that triggers, maintains, and augments the inflammation and progression of TF. We hypothesize that the "proliferation-death" circle is another important pathophysiologic mechanism of TF onset. Through this hypothesis, this paper interprets the development and progression of TF. Moreover, the vicious circle may be universal, underlying the development of inflammation and fibrosis in various organs and tissues. The hypothesis also suggests a potential therapy strategy for the inhibition of fibrosis.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Chen BC,Bai YH,Tang LL,Wang BQ,Liu B,Cai Y,Peng X,Yang YR,Zheng SLdoi
10.1016/j.mehy.2014.01.014subject
Has Abstractpub_date
2014-06-01 00:00:00pages
643-7issue
6eissn
0306-9877issn
1532-2777pii
S0306-9877(14)00025-5journal_volume
82pub_type
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