SARS-CoV FIBROSIS

Pathway ID: SIGNOR-SCFIView in NDEx

Description: Pulmonary fibrosis is a common consequence of SARS coronavirus (SARS-CoV) infection. Transforming growth factor-β1 (TGF-β1) is a crucial mediator of this phenomenon and causes tissue fibrosis by activating downstream small mother against decapentaplegic (Smad) signaling which triggers pro-fibrotic genes overexpression. Smad3 is the major downstream regulator that promote TGF-β mediated tissue fibrosis, while Smad7 protects against fibrosis inhibiting the TGF-β1/Smad pathway. The renin-angiotensin system (RAS) also controls the fibrotic process. The Spike-dependent down-regulation of ACE2 receptor decreases the Ang (1-7) level, upregulating the angiotensin-converting enzyme (ACE)- Ang II-angiotensin type 1 receptor (AT1R) signalling cascade, which in turn triggers inflammation and fibrosis in pulmonary tissue.

Curated by: Marta Iannuccelli

30 Seed Entities

Organism:
Name Primary ID
NfKb-p65/p50 SIGNOR-C13
N P59595
S P59594
Apoptosis SIGNOR-PH2
ACE P12821
S P0DTC2
Angiotensin-1 P01019-PRO_0000032457
chloroquine CHEBI:3638
Inflammation SIGNOR-PH12
TGFb SIGNOR-PF5
Alamandine CID:44192273
CGP-42112A CHEBI:147302
Fibrosis SIGNOR-PH90
SMAD3 P84022
Angiotensin-2 P01019-PRO_0000032458
SERPINE1 P05121
REN P00797
MRGPRD Q8TDS7
Angiotensin 1-7 P01019-PRO_0000420660
SMAD3/SMAD4 SIGNOR-C9
MAS1 P04201
EP300 Q09472
ACE2 Q9BYF1
TGFBR2 P37173
AGTR2 P50052
SMAD7 O15105
AGTR1 P30556
BCL2L11 O43521
AGT P01019
TGFBR1 P36897