Bahram Alamdary Badlou: Why Jak Inhibitors Demand Careful Monitoring In Chronic Inflammation Treatment?

Bahram Alamdary Badlou, Managing Director at BBAdvies and Research, shared Cüneyt Çetin‘s post on LinkedIn:

“Post COVID-19 war era (Updates November 2026) Research and Developments by Hedayati and Badlou et al. 2020-2024, together with broader international investigations, supports the concept that the cytokine-calcium-UPR axis represents a critical regulatory framework for understanding (pro-anti)inflammation, (pro-anti)thrombosis, and host defense.

Rather than viewing cytokines as simple messengers traveling toward the Nucleus/genome, modern biology increasingly recognizes (pro-anti)inflammation as a multidimensional network in which calcium signaling, platelet (hyper/hypo)activities (AsadiFar and Badlou et al 2015), RBCs’ participation(a-nucleus cells), and UPR governance collectively determine cellular fate and (patho)physiological outcome, after (pro-anti) inflammatory responses, in vivo, as we observed during and POSTCOVID-19 /POSTEBOLA 2026 viral attaks eras. (BBADVIES and RESEARCH 2010-2026, different R&Ds from bench to bed, partly published due to Patent-sensitive info…)”

Cüneyt Çetin, Senior Account Manager  at CooperSurgical Fertility Solutions, shared a post on LinkedIn:

“The JAK-STAT pathway: the fastest communication system in immunology.

Cells cannot read a cytokine directly.

A message that arrives at the cell surface has to be carried inside, and in immunology the quickest route from the membrane to the genome is the JAK-STAT pathway.

It translates extracellular signals directly into changes in gene expression, and in doing so it regulates inflammation, immunity, blood cell formation, proliferation, differentiation, and cell death.

The mechanism follows a clear sequence.

A cytokine binds its receptor on the cell surface.

This activates the Janus kinases, or JAKs, attached to the receptor, which phosphorylate it and create docking sites.

STAT proteins bind there and are themselves phosphorylated.

They then pair into dimers, travel into the nucleus, and bind DNA to switch specific genes on or off.

The result is a transcriptional response, which may include an inflammatory one.

A broad range of signals use this route. Interleukins such as IL-2, IL-4, IL-6, IL-7, IL-10, IL-12, and IL-23 depend on it, as do the interferons, erythropoietin, and growth hormone.

That breadth explains why one pathway can influence immunity, red cell production, and growth at once.

Its clinical significance is considerable.

Overactive or dysregulated signaling contributes to autoimmune disease and chronic inflammation, and it is implicated in cytokine storm.

Mutations in JAK2 are a hallmark of myeloproliferative neoplasms, and the pathway is involved in some hematologic malignancies.

It is also a therapeutic target.

JAK inhibitors such as tofacitinib, baricitinib, and ruxolitinib are used in conditions including rheumatoid arthritis and myelofibrosis, among others.

Because they act broadly on immune signaling, they carry risks, including infection, so they require careful selection and monitoring.

In reproductive biology, JAK-STAT signaling also contributes to implantation, where leukemia inhibitory factor acts through this pathway at the maternal-fetal interface.

One receptor, one kinase, one transcription factor, and a message delivered to the genome.

Thanks for making video under_thecoverslip”

Proceed to the video attached to the post.

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