Finding. NGF pain is two circuits. Neuronal TrkA carries the flinch and the heat. Schwann-cell p75NTR carries the lasting mechanical allodynia and cold hypersensitivity. On those glia, NGF and proNGF open a calcium-TRPA1-mitochondrial ROS-NOX1 loop. Kill ROS, kill TRPA1, or delete Schwann-cell Trpa1 and the persistent half dies while the TrkA half walks away. Cleavage-resistant proNGF never recruits the TrkA half at all.
Why this paper matters
Anti-NGF drugs were built on neuronal TrkA. This paper says the pain people actually hate living with (mechanical, cold, persistent) can be a Schwann-cell p75NTR problem with a mitochondrial ROS amplifier. That is a cell-type rewrite, not a ligand rewrite.
proNGF as a selective mechanical/cold agonist is a useful tool sentence. It also hints that precursor-versus-mature NGF ratios in tissue could pick which circuit is on.
What they actually measured
Behavior after NGF versus proNGF. Pharmacological and cell-specific genetics for TrkA versus p75NTR. Schwann-cell calcium, TRPA1, mitochondrial ROS, NOX1. Schwann-specific Trpa1 deletion. Endpoint split holds.
Mitochondrial ROS is a measured requirement, not a mapped complex.
How to read the score
Low seventies. Clean split, organelle ROS on the persistent path. Confidence is medium. Score 73.
What to do with it
If you work on NGF pain, Schwann cells, or TRPA1, pull the cell-specific genetics and the mtROS/NOX1 loop. Do not stop neuronal TrkA programs based on this brief; they still own acute and heat. The directional implication is that persistent NGF pain can be glial, oxidative, and mitochondrial without being neuronal TrkA.