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April 29, 2026Journal of Translational MedicineOpen Access

Cinacalcet attenuates nicotine-induced cardiac fibrosis by suppressing the METTL14/HNRNPA2B1/miR-125b-5p signaling pathway.

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Why the study?

The direct effects of nicotine on cardiac fibroblast biology and the molecular mechanisms underlying nicotine-induced cardiac fibrosis remained incompletely understood.

Population

Primary cardiac fibroblasts and a rat model of nicotine exposure

Comparison

Nicotine exposure and pathway manipulations vs controls

Design

In vitro and in vivo preclinical mechanistic study

Key result

Cinacalcet HCl effectively attenuated nicotine-induced cardiac fibrosis by suppressing the METTL14/HNRNPA2B1/miR-125b-5p signaling pathway.

Authors

HWHui‐Hui WuYLY. P. LiFMF. M. Meng

Discussion

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Overview

Nicotine avoidance remains key in at-risk cardiac patients; leaves open HNRNPA2B1/miR-125b-5p targeting for clinical validation.**[[1]](https://link.springer.com/article/10.

Key Points

  • This research aims to elucidate the molecular mechanisms by which nicotine promotes cardiac fibrosis and evaluate potential therapeutic interventions.
  • Utilized primary cardiac fibroblasts and a rat model to assess nicotine's pro-fibrotic effects.
  • Employed drug affinity responsive target stability (DARTS) and cellular thermal shift assay (CETSA) to identify nicotine's cellular targets.
  • Conducted miRNA biogenesis and m6A modification analyses through MeRIP and qRT-PCR.
  • Nicotine increased miR-125b-5p maturation via an HNRNPA2B1-mediated mechanism, resulting in accelerated cardiac fibrosis.
  • HNRNPA2B1 knockdown significantly lowered miR-125b-5p levels and alleviated nicotine-induced fibrotic properties.
  • Treatment with cinacalcet HCl effectively reduced cardiac fibrosis in both in vitro and in vivo models.

Structured PICO

P
Population
Primary cardiac fibroblasts (CFs) and a rat model of nicotine exposure
I
Intervention
Nicotine exposure, with or without miR-125b-5p overexpression/inhibition, HNRNPA2B1 silencing, or pharmacological inhibition with cinacalcet HCl
C
Comparator
Control (untreated/vehicle)
O
Outcome
Cardiac fibrosis (assessed by collagen deposition, CFs proliferation, myofibroblast transformation, and activated TGF-β1/MAPK signaling)surrogate

Cinacalcet HCl or HNRNPA2B1 knockdown attenuates nicotine-induced cardiac fibrosis by targeting the METTL14/m⁶A/miR-125b-5p axis.

Cite This Study

Wu et al. (2026) studied Cardiac fibrosis. Cinacalcet HCl vs. Nicotine alone was evaluated on Cardiac fibrosis and fibroblast proliferation. Cinacalcet HCl effectively attenuated nicotine-induced cardiac fibrosis by suppressing the METTL14/HNRNPA2B1/miR-125b-5p signaling pathway.

synapsesocial.com/papers/69f19f9cedf4b4682480654chttps://doi.org/10.1186/s12967-026-08184-0
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