Association Study of cAMP/EPACs Signaling Pathway Markers in Chronic Lumbar Pain in Dolisie (Congo)
Chronic low back pain represents a major public health issue, particularly in sub-Saharan Africa where it remains understudied. This cross-sectional case-control study, conducted in Dolisie (Congo), evaluated the involvement of cAMP/EPACs pathway markers (cyclic adenosine monophosphate and EPAC1/EPAC2 proteins) in low back pain. Seventy-five patients with chronic low back pain (pain duration ≥6 months, VAS score ≥30 mm) and 25 healthy controls were included. Intracellular concentrations of cAMP, EPAC1, and EPAC2 were measured in blood mononuclear cells (PBMCs) by ELISA, and pain intensity was measured using a visual analog scale (VAS). Analysis of our data showed a significant increase in cAMP (12.6 ± 2.1 for DL group against 3.2 ± 0.4 pmol/ml for TS group), EPAC1 (7.9 ± 1.2 for DL group against 2.1 ± 0.3 ng/ml for TS group) and EPAC2 (4.8 ± 0.7 for DL group against 1.5 ± 0.2 ng/ml for TS group) levels with a p-value < 0.0001 for the three markers compared. EPAC1 was more expressed than EPAC2, suggesting a predominant role in pain modulation. However, no significant correlation was observed between these biomarkers and VAS scores (p > 0.05), indicating that their activation reflects a pathophysiological mechanism without a direct link to subjective pain intensity. This study reveals dysregulation of the cAMP/EPACs pathway in chronic low back pain, opening up avenues for translational research targeting EPAC1 in a Congolese context. Limitations include the lack of clinical-biological correlation and the need for longitudinal studies to establish a causal link.
Authors
- M. Inana
- G. Loubano-Voumbi
- J. Ibinda
- J. Biazo
- C. R. Boumba Makaya
- C. Bademba
- B. Ndala
- E. Goma-Kouahi
Publication Details
- Journal
- African Journal of Biology and Medical Research
- Published
- 2025-08-14
- DOI
- https://doi.org/10.52589/ajbmr-mxper71s
- Primary Topic
- Phosphodiesterase function and regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.00