Perspective: Speculative role of Tmp21 mediated protein secretory pathway during endoplasmic reticulum (ER) stress induced chronic inflammation

TL;DR

This paper hypothesizes that Tmp21-mediated protein secretion during ER stress may contribute to chronic inflammation in myelofibrosis, suggesting a novel pathway involved in disease progression.

Contribution

It proposes a new speculative role for Tmp21 in ER stress-induced protein secretion and chronic inflammation in myelofibrosis, not previously elucidated.

Findings

Tmp21 may induce aberrant protein secretion during ER stress.

Increased Tmp21 availability could contribute to pathological inflammation.

Potential link between Tmp21 activity and disease progression in myelofibrosis.

Abstract

By deploying myelofibrosis as the disease context, I wish to propose that increased availability of Tmp21 (an NFAT gene target) induces aberrant protein secretion from the ER contributing to pathological consequences, which has not been elucidated before. Primary myelofibrosis is now mainly considered as an advanced stage of BCR-ABL1 negative myeloproliferative neoplasms (MPN), which otherwise include polycythemia vera and essential thrombocythemia. Myelofibrosis is defined by an increased insoluble collagen fiber deposition in the bone marrow2 and harbors chronic inflammation as an important component in disease progression.