Shared Mechanisms in Cancer and #CVD : #S100A8/9 and the #NLRP3 #Inflammasome
#CardioSky #OncoSky @cardioobdoc.bsky.social @novitham.bsky.social @pnatarajanmd.bsky.social
Shared Mechanisms in Cancer and #CVD : #S100A8/9 and the #NLRP3 #Inflammasome
#CardioSky #OncoSky @cardioobdoc.bsky.social @novitham.bsky.social @pnatarajanmd.bsky.social
www.biorxiv.org/content/10.6...
www.biorxiv.org/content/10.6...
We asked: what upstream signal ignites the inflammatory cycle that drives clonal hematopoiesis (CH)?
Answer: neutrophil-derived S100A8/A9 alarmins.
biorxiv.org/content/10.648
98/2026.06.26.734778v1
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We asked: what upstream signal ignites the inflammatory cycle that drives clonal hematopoiesis (CH)?
Answer: neutrophil-derived S100A8/A9 alarmins.
biorxiv.org/content/10.648
98/2026.06.26.734778v1
🧵1/4
Arthritis Care & Research
doi.org/10.1002/acr....
#Medsky #Rheumsky #lupus
Arthritis Care & Research
doi.org/10.1002/acr....
#Medsky #Rheumsky #lupus
Bin Gao & team show macrophages promote fat redistribution from adipocytes to hepatocytes and development of steatotic liver disease: www.jci.org/articles/vie...
The figure shows MASH liver has elevated S100A8+ macrophages.
Bin Gao & team show macrophages promote fat redistribution from adipocytes to hepatocytes and development of steatotic liver disease: www.jci.org/articles/vie...
The figure shows MASH liver has elevated S100A8+ macrophages.
www.nature.com/articles/s42...
www.nature.com/articles/s42...
#Calprotectin
www.mdpi.com/1422-0067/26...
#Calprotectin
www.mdpi.com/1422-0067/26...
'Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome'
#oncosky #cardiosky #cvprev
www.jacc.org/doi/10.1016/...
'Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome'
#oncosky #cardiosky #cvprev
www.jacc.org/doi/10.1016/...
Patients with higher GDF15 had worse fatigue scores.
Those with lower 12,13-diHOME had more physical fatigue and reduced activity.
Inflammation markers like S100A8 also tracked with fatigue and motivation loss.
Patients with higher GDF15 had worse fatigue scores.
Those with lower 12,13-diHOME had more physical fatigue and reduced activity.
Inflammation markers like S100A8 also tracked with fatigue and motivation loss.
Proteins like C1r, CFHR4, and S100A8 rose - linked to inflammation, fatigue, and brain dysfunction.
Calcium signaling, key to immune and brain function, was also disrupted.
Proteins like C1r, CFHR4, and S100A8 rose - linked to inflammation, fatigue, and brain dysfunction.
Calcium signaling, key to immune and brain function, was also disrupted.
doi.org/10.1002/acr....
S100A8/A9 levels elevated in SLE patients with cognitive impairment
doi.org/10.1002/acr....
doi.org/10.1002/acr....
S100A8/A9 levels elevated in SLE patients with cognitive impairment
doi.org/10.1002/acr....
Read more: doi.org/10.1007/s115...
#currentmedicalscience #Oncology #CancerTherapeutics
Read more: doi.org/10.1007/s115...
#currentmedicalscience #Oncology #CancerTherapeutics
"Inhibition of S100a8/a9 significantly improved mitochondrial function and alleviated muscle atrophy."
"Conversely, administration of recombinant S100a8/a9 protein exacerbated mitochondrial energy exhaustion and myocyte atrophy."
"Inhibition of S100a8/a9 significantly improved mitochondrial function and alleviated muscle atrophy."
"Conversely, administration of recombinant S100a8/a9 protein exacerbated mitochondrial energy exhaustion and myocyte atrophy."
#CardioSky #Calprotectin #S100A8/A9 #HeartFailure
www.ahajournals.org/doi/10.1161/...
#CardioSky #Calprotectin #S100A8/A9 #HeartFailure
www.ahajournals.org/doi/10.1161/...
www.science.org/doi/10.1126/...
www.science.org/doi/10.1126/...
"Mechanistically, S100a8/a9 binding to RAGE induced Drp1 phosphorylation and mitochondrial fragmentation, resulting in muscle atrophy."
"Mechanistically, S100a8/a9 binding to RAGE induced Drp1 phosphorylation and mitochondrial fragmentation, resulting in muscle atrophy."
"Our findings indicated the pivotal role of S100a8/a9 in driving the mitochondrial fragmentation in septic muscle atrophy."
"Our findings indicated the pivotal role of S100a8/a9 in driving the mitochondrial fragmentation in septic muscle atrophy."
"Targeting S100a8/a9-RAGE-initiated mitochondrial fission might offer a promising therapeutic intervention against septic muscle atrophy."
"Targeting S100a8/a9-RAGE-initiated mitochondrial fission might offer a promising therapeutic intervention against septic muscle atrophy."