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TheLaw's avatar

I have been collecting studies since the beginning of the pandemic, so have quite a long list. While not exhaustive, I have been saving the most important ones (to me) in a goggle doc:

https://docs.google.com/document/d/10qDWzHN9cfLeRkn3WvOVeVVY_t_zQgoMjUaalJezRPg/edit

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zuFpM5*M's avatar

I'm not a scientist, but I have been collecting these links. Sorry, I don't have time to format them properly.

“In the current study, we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.”

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2

Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan, John Y-J. Shyy See fewer authors

Originally published31 Mar 2021

https://doi.org/10.1161/CIRCRESAHA.121.318902

Circulation Research. 2021;128:1323–1326

“In this paper, we have shown that the SARS-CoV-2 S1 RBD binds to a number of aggregation-prone, heparin binding proteins including Aβ, α-synuclein, tau, prion, and TDP-43 RRM. These interactions suggests that the heparin-binding site on the S1 protein might assist the binding of amyloid proteins to the viral surface and thus could initiate aggregation of these proteins and finally leads to neurodegeneration in brain.”

SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration

Danish Idrees 1, Vijay Kumar 2

Affiliations expand

PMID: 33789211 PMCID: PMC7988450 DOI: 10.1016/j.bbrc.2021.03.100

https://pubmed.ncbi.nlm.nih.gov/33789211/

“Key to our findings is the demonstration that S1 promotes loss of barrier integrity in an advanced 3D microfluidic model of the human BBB, a platform that more closely resembles the physiological conditions at this CNS interface. Evidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function.”

The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier

Author links open overlay panelTetyana P.BuzhdyganabBrandon J.DeOrecAbigailBaldwin-LeclaircTrent A.BullockabHannah M.McGaryaJana A.KhanaRoshanakRazmpouraJonathan F.HaleaPeter A.GaliecRaghavaPotulaabAllison M.AndrewsabServio H.Ramirez

https://www.sciencedirect.com/science/article/pii/S096999612030406X

Preprint:

“We conclude that SARS-CoV-2 spike glycoprotein, efficiently primed, activated and strategically poised during biosynthesis, can exploit the CM's inherent membranous connectivity to drive heart damage directly, uncoupling clinically common myocardial injury from lymphocytic myocarditis, often suspected but rarely confirmed in COVID-19.”

SARS-CoV-2 direct cardiac damage through spike-mediated cardiomyocyte fusion

Jay W. Schneider 1 # , David R. Pease 1 #, Chanakha K. Navaratnarajah 2 #, Peter Halfmann 3, Daniel J. Clemens 4, Dan Ye 4, 5, Chang Sung Kim 4, 5, Alison Barkhymer 2, Stephen Cohle 6, Aron Banks 7, Arpit Mehta 7, Joseph Rantus 7, Tim L. Emmerzaal 8, Tamás Kozicz 8, Kyle G. Howell 9, Jon E. Charlesworth 9, Trace A. Christensen 9, Yoshihiro Kawaoka 3, 10, Leslie T. Cooper 11, Michael J. Ackerman 4, 5, Roberto Cattaneo 2, and Wanek Family Program for HLHS-Stem Cell Pipeline

https://europepmc.org/article/ppr/ppr232448

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