PMID- 31936109
OWN - NLM
STAT- MEDLINE
DCOM- 20210331
LR  - 20210331
IS  - 2218-273X (Electronic)
IS  - 2218-273X (Linking)
VI  - 10
IP  - 1
DP  - 2020 Jan 7
TI  - Autophagy Function and Regulation in Kidney Disease.
LID - 10.3390/biom10010100 [doi]
LID - 100
AB  - Autophagy is a dynamic process by which intracellular damaged macromolecules and 
      organelles are degraded and recycled for the synthesis of new cellular 
      components. Basal autophagy in the kidney acts as a quality control system and is 
      vital for cellular metabolic and organelle homeostasis. Under pathological 
      conditions, autophagy facilitates cellular adaptation; however, activation of 
      autophagy in response to renal injury may be insufficient to provide protection, 
      especially under dysregulated conditions. Kidney-specific deletion of Atg genes 
      in mice has consistently demonstrated worsened acute kidney injury (AKI) outcomes 
      supporting the notion of a pro-survival role of autophagy. Recent studies have 
      also begun to unfold the role of autophagy in progressive renal disease and 
      subsequent fibrosis. Autophagy also influences tubular cell death in renal 
      injury. In this review, we reported the current understanding of autophagy 
      regulation and its role in the pathogenesis of renal injury. In particular, the 
      classic mammalian target of rapamycin (mTOR)-dependent signaling pathway and 
      other mTOR-independent alternative signaling pathways of autophagy regulation 
      were described. Finally, we summarized the impact of autophagy activation on 
      different forms of cell death, including apoptosis and regulated necrosis, 
      associated with the pathophysiology of renal injury. Understanding the regulatory 
      mechanisms of autophagy would identify important targets for therapeutic 
      approaches.
FAU - Kaushal, Gur P
AU  - Kaushal GP
AD  - Renal Section, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 
      and Division of Nephrology, 4300 W 7th St, Little Rock, AR 72205, USA.
AD  - Department of Internal Medicine, University of Arkansas for Medical Sciences, 
      4301 W. Markham, Little Rock, AR 72205, USA.
FAU - Chandrashekar, Kiran
AU  - Chandrashekar K
AD  - Department of Internal Medicine, University of Arkansas for Medical Sciences, 
      4301 W. Markham, Little Rock, AR 72205, USA.
FAU - Juncos, Luis A
AU  - Juncos LA
AUID- ORCID: 0000-0002-4630-2747
AD  - Renal Section, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 
      and Division of Nephrology, 4300 W 7th St, Little Rock, AR 72205, USA.
AD  - Department of Internal Medicine, University of Arkansas for Medical Sciences, 
      4301 W. Markham, Little Rock, AR 72205, USA.
FAU - Shah, Sudhir V
AU  - Shah SV
AD  - Renal Section, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 
      and Division of Nephrology, 4300 W 7th St, Little Rock, AR 72205, USA.
AD  - Department of Internal Medicine, University of Arkansas for Medical Sciences, 
      4301 W. Markham, Little Rock, AR 72205, USA.
LA  - eng
GR  - BX000444/VA Aministration/International
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
DEP - 20200107
PL  - Switzerland
TA  - Biomolecules
JT  - Biomolecules
JID - 101596414
SB  - IM
MH  - Acute Kidney Injury/metabolism/*pathology/therapy
MH  - Animals
MH  - Apoptosis
MH  - Autophagy/*physiology
MH  - Fibrosis
MH  - Homeostasis
MH  - Humans
MH  - Kidney/pathology
MH  - Kidney Diseases/*physiopathology
MH  - Signal Transduction
PMC - PMC7022273
OTO - NOTNLM
OT  - AMPK
OT  - acute kidney injury
OT  - apoptosis
OT  - autophagy
OT  - chronic kidney disease
OT  - diabetic nephropathy
OT  - mTORC1
OT  - regulated necrosis
OT  - renal fibrosis
COIS- The authors declare no conflict of interest.
EDAT- 2020/01/16 06:00
MHDA- 2021/04/01 06:00
PMCR- 2020/01/01
CRDT- 2020/01/16 06:00
PHST- 2019/11/27 00:00 [received]
PHST- 2019/12/16 00:00 [revised]
PHST- 2019/12/19 00:00 [accepted]
PHST- 2020/01/16 06:00 [entrez]
PHST- 2020/01/16 06:00 [pubmed]
PHST- 2021/04/01 06:00 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - biom10010100 [pii]
AID - biomolecules-10-00100 [pii]
AID - 10.3390/biom10010100 [doi]
PST - epublish
SO  - Biomolecules. 2020 Jan 7;10(1):100. doi: 10.3390/biom10010100.