ReviewFrontiers in cell and developmental biology2026
Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipid droplets and mitochondria form regulated contact sites whose molecular composition, phosphorylation state and spatial geometry now behave as measurable, druggable variables in living cells. The molecular toolkit has been mapped in liver, muscle and adipose tissue, yet its application to respiratory disease has lagged despite a lung-specific dependence on lipid biology that spans surfactant biogenesis, alveolar-macrophage lipid handling and fibroblast-driven remodelling. This review argues that the lipid-droplet-mitochondria contact site is an emerging spatial-pharmacology target in respiratory medicine, and organises the evidence into a three-way matrix with explicit grading of direct, indirect and cross-tissue evidence. A common molecular toolkit built around perilipin-family scaffolds, mitochondrial-outer-membrane tethers, an endoplasmic-reticulum bridging apparatus and the PFKL-PLIN2-CPT1A flux node (mechanistically established in hepatocellular carcinoma and inferred in lung) is rewired into cell-type-specific configurations across alveolar type 2 cells, macrophages, fibroblasts, endothelium and lung adenocarcinoma. That toolkit acquires a distinct disease role across idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, asthma, acute respiratory distress syndrome, tuberculosis, severe acute respiratory syndrome coronavirus two infection and lung cancer, generating a matrix of cell-type-by-disease configurations that no prior review has systematized. Four target axes, namely, tether occupancy, lipid flux, redox coupling and cell-type-precise delivery, converge geometrically at the interface and motivate combination strategies rather than pan-mitochondrial single-agent approaches. Inhaled lipid nanoparticles, mucus-penetrating carriers and engineered extracellular vesicles bring these targets within reach with cell-type precision. Endothelial contact-site biology is identified as the largest evidence gap and discussed candidly. The framework is offered as a roadmap for tether-axis compound development, contact-site engagement biomarkers and dual-axis inhaled therapeutics.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.