Alex Genzelinakh

98 posts

Alex Genzelinakh

Alex Genzelinakh

@genzelinakh

PhD student in biology. Intrigued by extracellular vesicles. Love spending time with my wife and cat (2 different entities). @Tzahor_Lab #Vesicles #regeneration

Israel Katılım Eylül 2019
164 Takip Edilen66 Takipçiler
Alex Genzelinakh retweetledi
Shoval Miyara
Shoval Miyara@MiyaraShoval·
I'm so excited this episode of @MotionPod is finally out!! I had a blast chatting and diving deep into hot🔥 and cold❄️ #fibrosis in light of our recent @biorxivpreprint with @JACoates. Thanks for having me! biorxiv.org/content/10.110…
Preprints in Motion podcast@MotionPod

Latest episode out now 🎉. It even includes a terrible terrible joke by me right at the start! Hot and cold fibrosis with @MiyaraShoval listen here -> pod.fo/e/173857

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Eldad Tzahor
Eldad Tzahor@Tzahore·
Here we show for the first time the utility of our circuit to target approach- relying on mechanistic yet simple mathematical models of complex #disease states and identifying new therapeutic targets!
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Targeting of Timp1 using neutralizing antibodies reduced fibrosis after MI in adult mice 🐭13/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Using #NicheNet and in-vitro experiments we identified Timp1 as a novel autocrine growth factor for cardiac myofibroblasts 12/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
We further asked which molecular interactions might be suitable targets for reducing cold❄️fibrosis. We suggest that inhibiting the myofibroblast autocrine growth-factor signaling could reduce cold❄️fibrosis 11/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
We next asked whether cold❄️fibrosis is characterized by cell fate changes. Using #Pareto analysis, we find that #fibroblasts acquire a novel fibrotic function associated with ECM remodeling while macrophages return to baseline homeostatic functions 10/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Using RNAseq and histological analysis we show that cold❄️fibrosis is a conserved outcome in pigs🐖. We further show that administration of the ECM protein Agrin largely reverses cold❄️fibrosis into a healing state 9/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Using #Visium we show that macrophages are reduced specifically at the infarct zone between 7-14 days while myofibroblasts remain. Interestingly, we also find that the border zone is reduced when cold❄️fibrosis sets in 8/
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Alex Genzelinakh retweetledi
Eldad Tzahor
Eldad Tzahor@Tzahore·
Following MI, both macrophages and myofibroblasts rise together followed by a decline in macrophage numbers, while myofibroblasts persist- suggesting that MI leads to cold❄️fibrosis 7/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Recently, @MiriAdler @UriAlonWeizmann published a mathematical model for a macrophage-myofibroblasts cell circuit that predicts two types of #fibrosis- hot🔥fibrosis with both cell types supporting each other, and cold❄️fibrosis dominated by myofibroblasts 5/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
#Fibrosis is a pathology of excessive #ECM deposition. It is immensely complex and involves multiple cell types, and molecules, and it continues to develop over time⏰. To develop new therapeutic approaches, it's crucial to simplify the underlying concepts 4/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
🏃Briefly, here we combined mathematical #modeling and in-vivo studies to establish a new approach to determine the tissue fate after injury: fibrosis vs healing. We describe a new strategy to identify therapeutic targets to reduce #fibrosis 2/
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Eldad Tzahor
Eldad Tzahor@Tzahore·
Happy new year 🥂🎉🎇 Our first preprint for 2023 is now OUT in @BioRxiv! Circuit to target approach defines an autocrine myofibroblast loop that drives cardiac fibrosis 1/ biorxiv.org/content/10.110…
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