PMID- 32088215
OWN - NLM
STAT- MEDLINE
DCOM- 20200409
LR  - 20200409
IS  - 1879-0631 (Electronic)
IS  - 0024-3205 (Linking)
VI  - 247
DP  - 2020 Apr 15
TI  - Clearing or subverting the enemy: Role of autophagy in protozoan infections.
PG  - 117453
LID - S0024-3205(20)30201-0 [pii]
LID - 10.1016/j.lfs.2020.117453 [doi]
AB  - The protozoan parasites are evolutionarily divergent, unicellular eukaryotic 
      pathogens representing one of the essential sources of parasitic diseases. These 
      parasites significantly affect the economy and cause public health burdens 
      globally. Protozoan parasites share many cellular features and pathways with 
      their respective host cells. This includes autophagy, a process responsible for 
      self-degradation of the cell's components. There is conservation of the central 
      structural and functional machinery for autophagy in most of the eukaryotic 
      phyla, however, Plasmodium and Toxoplasma possess a decreased number of 
      recognizable autophagy-related proteins (ATG). Plasmodium noticeably lacks clear 
      orthologs of the initiating kinase ATG1/ULK1/2, and both Plasmodium and 
      Toxoplasma lack proteins involved in the nucleation of autophagosomes. These 
      organisms have essential apicoplast, a plastid-like non-photosynthetic organelle, 
      which is an adaptation that is used in penetrating the host cell. Furthermore, 
      available evidence suggests that Leishmania, an intracellular protozoan parasite, 
      induces autophagy in macrophages. The autophagic pathway in Trypanosoma cruzi is 
      activated during metacyclogenesis, a process responsible for the infective forms 
      of parasites. Therefore, numerous pathogens have developed strategies to impair 
      the autophagic mechanism in phagocytes. Regulating autophagy is essential to 
      maintain cellular health as adjustments in the autophagy pathway have been linked 
      to the progression of several physiological and pathological conditions in 
      humans. In this review, we report current advances in autophagy in parasites and 
      their host cells, focusing on the ramifications of these studies in the design of 
      potential anti-protozoan therapeutics.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Ghartey-Kwansah, George
AU  - Ghartey-Kwansah G
AD  - Department of Biomedical Sciences, College of Health and Allied Sciences, 
      University of Cape Coast, Cape Coast, Ghana; College of Life Sciences, Shaanxi 
      Normal University, Xi'an 710119, China. Electronic address: ggk2014@snnu.edu.cn.
FAU - Aboagye, Benjamin
AU  - Aboagye B
AD  - Department of Forensic Sciences, College of Agriculture and Natural Sciences, 
      University of Cape Coast, Cape Coast, Ghana.
FAU - Adu-Nti, Frank
AU  - Adu-Nti F
AD  - College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
FAU - Opoku, Yeboah Kwaku
AU  - Opoku YK
AD  - Department of Biology Education, Faculty of Science, University of Education, 
      Winneba, Ghana.
FAU - Abu, Emmanuel Kwasi
AU  - Abu EK
AD  - Department of Optometry and Vision Science, College of Health and Allied 
      Sciences, University of Cape Coast, Cape Coast, Ghana.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200220
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Antiprotozoal Agents)
RN  - 0 (Autophagy-Related Proteins)
RN  - 0 (Protozoan Proteins)
SB  - IM
MH  - Animals
MH  - Antiprotozoal Agents/*therapeutic use
MH  - Apicoplasts/metabolism
MH  - Autophagosomes/metabolism
MH  - Autophagy/*drug effects
MH  - Autophagy-Related Proteins/metabolism
MH  - Eukaryota/drug effects/metabolism
MH  - Humans
MH  - Phagocytes/metabolism
MH  - Protozoan Infections/*drug therapy/*metabolism
MH  - Protozoan Proteins/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Autophagosome
OT  - Autophagy
OT  - LC3-associated phagocytosis (LAP)
OT  - Protozoan parasites
OT  - Xenophagy
COIS- Declaration of competing interest Authors declare no competing interest.
EDAT- 2020/02/24 06:00
MHDA- 2020/04/10 06:00
CRDT- 2020/02/24 06:00
PHST- 2020/01/02 00:00 [received]
PHST- 2020/02/17 00:00 [revised]
PHST- 2020/02/19 00:00 [accepted]
PHST- 2020/02/24 06:00 [pubmed]
PHST- 2020/04/10 06:00 [medline]
PHST- 2020/02/24 06:00 [entrez]
AID - S0024-3205(20)30201-0 [pii]
AID - 10.1016/j.lfs.2020.117453 [doi]
PST - ppublish
SO  - Life Sci. 2020 Apr 15;247:117453. doi: 10.1016/j.lfs.2020.117453. Epub 2020 Feb 
      20.