PMID- 36077377
OWN - NLM
STAT- MEDLINE
DCOM- 20220912
LR  - 20220913
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 23
IP  - 17
DP  - 2022 Sep 1
TI  - Nephritis-Associated Plasmin Receptor (NAPlr): An Essential Inducer of 
      C3-Dominant Glomerular Injury and a Potential Key Diagnostic Biomarker of 
      Infection-Related Glomerulonephritis (IRGN).
LID - 10.3390/ijms23179974 [doi]
LID - 9974
AB  - Nephritis-associated plasmin receptor (NAPlr) was originally isolated from the 
      cytoplasmic fraction of group A Streptococci, and was found to be the same 
      molecule as streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and 
      plasmin receptor (Plr) on the basis of nucleotide and amino acid sequence 
      homology. Its main functions include GAPDH activity, plasmin-binding capacity, 
      and direct activation of the complement alternative pathway (A-P). Plasmin 
      trapped by deposited NAPlr triggers the degradation of extracellular matrix 
      proteins, such as glomerular basement membranes and mesangial matrix, and the 
      accumulation of macrophages and neutrophils, leading to the induction of 
      plasmin-related endocapillary glomerular inflammation. Deposited NAPlr at 
      glomerular endocapillary site directly activates the complement A-P, and the 
      endocapillary release of complement-related anaphylatoxins, C3a and C5a, amplify 
      the in situ endocapillary glomerular inflammation. Subsequently, circulating and 
      in situ-formed immune complexes participate in the glomerular injury resulting in 
      NAPlr-mediated glomerulonephritis. The disease framework of infection-related 
      glomerulonephritis (IRGN) has been further expanded. GAPDH of various bacteria 
      other than Streptococci have been found to react with anti-NAPlr antibodies and 
      to possess plasmin-binding activities, allowing glomerular NAPlr and plasmin 
      activity to be utilized as key biomarkers of IRGN.
FAU - Yoshizawa, Nobuyuki
AU  - Yoshizawa N
AD  - Division of Nephrology, Showanomori Hospital, Tokyo 196-0024, Japan.
FAU - Yamada, Muneharu
AU  - Yamada M
AUID- ORCID: 0000-0003-0483-0012
AD  - Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo 
      Medical University Hachioji Medical Center, Tokyo 193-0998, Japan.
FAU - Fujino, Masayuki
AU  - Fujino M
AD  - National Institute of Infectious Disease, Tokyo 162-8640, Japan.
FAU - Oda, Takashi
AU  - Oda T
AD  - Department of Nephrology and Blood Purification, Kidney Disease Center, Tokyo 
      Medical University Hachioji Medical Center, Tokyo 193-0998, Japan.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220901
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Biomarkers)
RN  - 0 (Receptors, Peptide)
RN  - 0 (plasmin receptor)
RN  - EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases)
RN  - EC 3.4.21.7 (Fibrinolysin)
SB  - IM
MH  - Biomarkers
MH  - Fibrinolysin
MH  - *Glomerulonephritis/metabolism
MH  - Glyceraldehyde-3-Phosphate Dehydrogenases
MH  - Humans
MH  - Inflammation
MH  - *Nephritis
MH  - Receptors, Peptide
MH  - *Streptococcal Infections
PMC - PMC9456382
OTO - NOTNLM
OT  - C3-dominant glomerular injury
OT  - NAPlr (Bacterial GAPDH) mediated glomerulonephritis
OT  - immune complex-dominant glomerular injury
OT  - infection-related glomerulonephritis (IRGN)
OT  - nephritis-associated plasmin receptor (NAPlr)
OT  - poststreptococcal acute glomerulonephritis (PSAGN)
COIS- The authors declare no conflict of interest.
EDAT- 2022/09/10 06:00
MHDA- 2022/09/14 06:00
PMCR- 2022/09/01
CRDT- 2022/09/09 01:08
PHST- 2022/07/03 00:00 [received]
PHST- 2022/08/11 00:00 [revised]
PHST- 2022/08/16 00:00 [accepted]
PHST- 2022/09/09 01:08 [entrez]
PHST- 2022/09/10 06:00 [pubmed]
PHST- 2022/09/14 06:00 [medline]
PHST- 2022/09/01 00:00 [pmc-release]
AID - ijms23179974 [pii]
AID - ijms-23-09974 [pii]
AID - 10.3390/ijms23179974 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Sep 1;23(17):9974. doi: 10.3390/ijms23179974.