# Heat-Treated Lactiplantibacillus plantarum KM2 Fermentation Ameliorate Muscular Atrophy

**Authors:** Minji Kang, Minkyoung Kang, Moon-Hee Sung, Jong-Hoon Kim, Juyeon Lee, Kwangcheol Casey Jeong, Sangnam Oh

PMC · DOI: 10.4014/jmb.2506.06042 · Journal of Microbiology and Biotechnology · 2025-09-25

## TL;DR

A fermented product from Lactiplantibacillus plantarum KM2 may help prevent muscle loss in aging and cancer patients.

## Contribution

The study introduces a novel postbiotic formulation that shows muscle-preserving effects in model organisms.

## Key findings

- KLP_KM2 extended lifespan and improved movement in C. elegans.
- KLP_KM2 restored muscle cell size and expression of muscle markers in C2C12 cells.
- The treatment downregulated muscle atrophy markers in muscle cells.

## Abstract

Sarcopenia, a progressive loss of skeletal muscle mass and function, poses a significant health concern in aging populations and cancer patients. Despite ongoing pharmaceutical research, including drug repurposing strategies, no FDA-approved treatment is currently available for sarcopenia, highlighting the need for safer, food-derived interventions. This study evaluated the anti-aging and muscle-preserving effects of KLP_KM2, a postbiotic formulation derived from Lactiplantibacillus plantarum KM2, using Caenorhabditis elegans and C2C12 muscle cell models. In C. elegans, KLP_KM2 and its components significantly extended lifespan, reduced lipofuscin accumulation, enhanced pharyngeal pumping, and preserved coordinated movement patterns. These effects were accompanied by upregulation of longevity, immune/stress response, and muscle function-related genes. In C2C12 myotubes, KLP_KM2 treatment mitigated CT26-conditioned medium-induced muscle atrophy, restoring myotube diameter and length, increasing expression of myogenic markers (MyoD, myogenin, MHC I, MHC IIa), and downregulating atrophy markers (Atrogin-1, MuRF1). These findings suggest that KLP_KM2 may serve as a promising postbiotic intervention to support muscle health, prevent sarcopenia, and counteract cancer cachexia. Further in vivo mammalian studies and clinical trials are warranted to validate its therapeutic potential.

## Linked entities

- **Genes:** MYOD1 (myogenic differentiation 1) [NCBI Gene 4654], myog.S (myogenin S homeolog) [NCBI Gene 373806], MHC-I (BOLA class I histocompatibility antigen, alpha chain BL3-7) [NCBI Gene 100009719], LOC109196430 (H-2 class II histocompatibility antigen, A-U alpha chain) [NCBI Gene 109196430], Fbxo32 (F-box protein 32) [NCBI Gene 67731], TRIM63 (tripartite motif containing 63) [NCBI Gene 84676]
- **Species:** Caenorhabditis elegans (taxon 6239), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** FBXO32 (F-box protein 32) [NCBI Gene 114907] {aka Fbx32, MAFbx}, MYOD1 (myogenic differentiation 1) [NCBI Gene 4654] {aka CMYO17, CMYP17, MYF3, MYOD, MYODRIF, PUM}, TRIM63 (tripartite motif containing 63) [NCBI Gene 84676] {aka CMH31, IRF, MURF1, MURF2, RNF28, SMRZ}, MYOG (myogenin) [NCBI Gene 4656] {aka MYF4, bHLHc3, myf-4}
- **Diseases:** cancer (MESH:D009369), Muscular Atrophy (MESH:D009133), loss of skeletal muscle mass and function (MESH:C536030), Sarcopenia (MESH:D055948), atrophy (MESH:D001284)
- **Chemicals:** KLP_KM2 (-), lipofuscin (MESH:D008062)
- **Species:** C. elegans [taxon 328850], Caenorhabditis elegans (species) [taxon 6239], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** C2C12 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0188), CT26 — Mus musculus (Mouse), Mouse colon adenocarcinoma, Cancer cell line (CVCL_7254)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12535864/full.md

## Figures

12 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12535864/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC12535864/full.md

---
Source: https://tomesphere.com/paper/PMC12535864