Whenever I get confused I got back to this

.. and whenever I get confused, I go back to this 😅

Under some conditions, and I am open to this, this may permit crosstalk with other death machineries, but to the best of my judgement the evidence that it is simply upstream of apoptosis, cathepsin-dependent death, or other canonical programs remains unconvincing

But I think we may be moving toward a more nuanced view. “Ferroptosis” could be an umbrella term encompassing distinct organelle membranes, each controlled by distinct enzymatic and non-enzymatic protective systems.

In that setting, ferroptosis does not look to me like apoptosis or lysosomal cell death by another route.

That is why I have generally felt that placing ferroptosis among the necrotic forms of cell death was a useful approximation.

On mechanism, in many genetic screens, we have never seen a convincing contribution from apoptosis, cathepsins, or similar pathways, at least in clean systems where GPX4 inhibition is the initiating event.

There is also a "marketing" side to this discussion, it is easier to build attention, legitimacy, and funding around a “cell death pathway” than around a ROS-driven cellular event.

That does not make the biology any less important, but I do think the framing has partly been shaped by that dynamic.

Is it a distinct cell death pathway? I think that is a fair description, though I’m happy to leave the formal taxonomy to nomenclature-organizing colleagues in the cell death field.

😰 good Monday morning exercise 😰

My two cents on this - ferroptosis is best understood as a terminal process that begins once lipid oxidative damage exceeds the cell’s buffering and repair capacity.

Does it lead to cell death? Clearly yes.

would you also call them drug tolerant? I find sometime hard to follow on these nomenclatures and what they really mean -

Very grateful to receive the Deutscher Krebspreis 2026 (Experimental Cancer Research) together with Marcus Conrad. This recognition reflects the incredible efforts of our teams and collaborators over the years
@uni-wuerzburg.de

Pleased to share our recent work out today in @natmetabolism.nature.com. This study addresses a longstanding mystery - NRF2-driven cancers increase cysteine acquisition (via xCT) by ~5x - so where does all that cysteine go?

Uproar in Germany over law requiring men get military approval for long stays abroad Clause says those aged up to 45 may need permission from armed forces to leave country for more than three months

Uproar in Germany over law requiring men get military approval for long stays abroad

www.theguardian.com/world/2026/a...

If you are a postdoc or grad students that wants to be considered for a talk at the GRS then get your abstract in! (Deadline 5th April).

If a week by the Mediterranean discussing the latest research Bridging Redox Chemistry to Biology, Aging and Disease sounds like a welcome escape, then this Gordon Research Conference could be for you! www.grc.org/thiol-based-...

Excited to co-chair the 2026 Gordon Research Seminar (GRS) on Thiol-Based Redox Regulation & Signaling with Taylor Covington, a meeting for early career researchers in redox research

📍 Castelldefels (Barcelona), Spain ☀️
📅 July 11–12, 2026

#Redox #Thiols #EarlyCareerResearchers

More details ↓

Very grateful to receive the Deutscher Krebspreis 2026 (Experimental Cancer Research) together with Marcus Conrad. This recognition reflects the incredible efforts of our teams and collaborators over the years
@uni-wuerzburg.de

Isn't this like normal?

Riboflavin metabolism shapes FSP1-driven ferroptosis resistance - Nature Cell Biology After performing a focused CRISPR–Cas9 screen, Skafar et al. identify riboflavin (vitamin B2) as a regulator of FSP1 stability that modulates phospholipid peroxidation and ferroptosis sensitivity in c...

Happy to share the final version of the study where we describe a central role for vitaminB2 in regulating membrane redox state - some new cool experiments were added since the preprint was posted - pls check this out

thttps://www.nature.com/articles/s41556-025-01856-x

Interested in investigating dietary and metabolic regulation of immune responses? We have a PostDoc and a PhD position available in the lab.

karriereamukb.de/jobs/postdoc...

This is figure 5, which shows that the riboflavin antimetabolite roseoflavin disrupts FSP1 activity.

A study in Nature Cell Biology identifies riboflavin, vitamin B2, as a regulator of FSP1 stability that modulates phospholipid peroxidation and ferroptosis sensitivity in cancer cells. underscoring the therapeutic potential of targeting riboflavin metabolism. go.nature.com/4blD8Gi #medsky 🧪

Interesting and systematic evaluation that consolidates many observations the field has already been converging on: GPX4 dependency appears to be overestimated in vivo. Suggesting that exploiting high-PUFA states in specific cancer entities is unlikely to benefit from single-target GPX4 inhibition.

Interesting and systematic evaluation that consolidates many observations the field has already been converging on: GPX4 dependency appears to be overestimated in vivo. Suggesting that exploiting high-PUFA states in specific cancer entities is unlikely to benefit from single-target GPX4 inhibition.

Hei Derek!
Thanks a lot 😊

#Vitamin B2 is converted into molecules which protect cells from oxidative damage. The downside: It also protects #cancer cells. Scientists at the Rudolf Virchow Centre at #JMU discovered that. 📸 Natalie Fahmer
➡️ www.uni-wuerzburg.de/en/news-and-...

Vitamin B2 metabolism promotes FSP1 stability to prevent ferroptosis - Nature Structural & Molecular Biology Here, Deol et al. use genetic screens in gene-edited reporter cell lines to identify regulators of ferroptosis suppressor protein 1 (FSP1) expression and stability. They show that vitamin B2 metabolis...

also see the study from @olzmannlab.bsky.social who independently report on the importance of vitaminB2 on
ferroptosis

www.nature.com/articles/s41...

Riboflavin metabolism shapes FSP1-driven ferroptosis resistance - Nature Cell Biology After performing a focused CRISPR–Cas9 screen, Skafar et al. identify riboflavin (vitamin B2) as a regulator of FSP1 stability that modulates phospholipid peroxidation and ferroptosis sensitivity in c...

Happy to share the final version of the study where we describe a central role for vitaminB2 in regulating membrane redox state - some new cool experiments were added since the preprint was posted - pls check this out

thttps://www.nature.com/articles/s41556-025-01856-x

FAD-dependent stabilization of FSP1 promotes ferroptosis resistance Nature Structural & Molecular Biology, Published online: 13 March 2026; doi:10.1038/s41594-026-01760-4The oxidoreductase FSP1 recycles radical-trapping antioxidants that suppress oxidative lipid damage and ferroptosis. A series of genetic screens reveal a key role for the vitamin B2 metabolite flavin adenine dinucleotide in stabilizing FSP1, preventing its proteasomal degradation and promoting ferroptosis suppression.

New online: FAD-dependent stabilization of FSP1 promotes ferroptosis resistance

🧐 What if metabolic defects are not just a consequence of inflammatory disease - but actively contribute to it?

Inflammation and metabolism are deeply intertwined, but the molecular links remain unclear.

Our new paper in Cell Death & Differentiation uncovers one. 🧵👇
nature.com/articles/s41...

It's shaping up to be an amazing line up at the Gordon Cell Death meeting! Register now! www.grc.org/cell-death-c...