Zombie cells and mitochondrial mess might explain age inflammation
Posted by fasted_labrat in Longevity & Anti-Aging - 2 points, 4 comments.
Saw this one pop up about how senescent cells basically mess with their own mitochondria and that flips a switch that exposes inflammatory genes, which is wild because it gives a real mechanistic story for why aging feels like low grade garbage fire all the time.
The mitochondrial angle is what makes it interesting for me, not just another "zombie cells bad" paper. If the problem is partly about how energy production goes sideways and drags DNA packaging with it, that actually lines up with how NAD+ and metabolic stuff get talked about in longevity circles. It makes me wonder if hitting senolytics alone is even enough, or if you also need to clean up the mitochondrial side of things to calm the inflammation down properly.
Anyone following this line of research? Curious if this changes how people are thinking about stacking approaches, no?
Comments
- restless_optimizer: Yeah this one caught my eye too. The mito angle is what makes it worth more than the usual "senolytics fix aging" take imo. If the inflammatory signal is partly downstream of messed up cellular energetics, just clearing senescent cells without addressing that side seems like half a job. I've been curious whether that's part of why some people report feeling kind of meh on senolytic protocols alone. Or maybe its just timing and the mito cleanup happens once the senescent load drops. Hard to say
- fasted_labrat: Yeah exactly, the "half a job" framing is what keeps bugging me too. Like if the epigenetic switch only flips when mitochondria are already wrecked, then clearing the cell before the mito side catches up might just leave you with a clean cell that immediately re-senesces, right? Or am I overthinking it 🧠
- tiredmira: Yeah the energetics side is exactly what I keep circling back to. If the inflammatory cascade is downstream of ATP production going sideways, clearing senescent cells without touching NAD or mito function just feels incomplete to me. Would love to see someone actually run senolytics plus an NAD precursor and track CRP alongside HRV over a few months. Basically the kind of data that would tell us if the combo is doing anything or if the mito piece is just slowly fixing itself after senolytic loa
- fasted_labrat: Totally, I keep saying the same thing, like what good is clearing the cells if the metabolic garbage stays around and just recruits new ones right back in 😅 the NAD piece feels like the missing half, no?
Community discussion - research and educational context only. Not medical advice.