# Cardiovascular remodeling: key mechanisms and clinical implications linking sarcopenia and heart failure

**Authors:** Jinghong Yang, Xinyu Zhang, Jun Zhong

PMC · DOI: 10.3389/fmed.2026.1736824 · Frontiers in Medicine · 2026-02-12

## TL;DR

This paper explores how heart failure and muscle loss are linked through shared mechanisms like inflammation and how this understanding can lead to better treatments.

## Contribution

The paper provides a unified framework for the mechanistic links between sarcopenia and heart failure, highlighting novel therapeutic targets.

## Key findings

- Cardiovascular remodeling mediates the bidirectional relationship between sarcopenia and heart failure.
- Shared mechanisms include chronic inflammation, oxidative stress, and insulin resistance.
- Targeting these pathways could improve outcomes for both conditions.

## Abstract

Sarcopenia and heart failure (HF) are interconnected through a bidirectional relationship in which cardiovascular remodeling serves as a critical mediator. This review examines the shared pathophysiological mechanisms—such as chronic inflammation, oxidative stress, and insulin resistance—that underlie both conditions. By integrating recent clinical and experimental evidence, we emphasize the role of cardiovascular remodeling in aggravating muscle loss in sarcopenia and cardiac dysfunction in HF. Furthermore, we discuss novel therapeutic targets directed at disrupting these common pathways. This analysis offers a unified framework for understanding the mechanistic links between sarcopenia and HF, with implications for future research and clinical strategies aimed at enhancing patient outcomes.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** SREBF1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 6720] {aka HMD, IFAP2, SREBP1, bHLHd1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, MYC (MYC proto-oncogene, bHLH transcription factor) [NCBI Gene 4609] {aka MRTL, MYCC, bHLHe39, c-Myc}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, DKK3 (dickkopf Wnt signaling pathway inhibitor 3) [NCBI Gene 27122] {aka CRRL, REIC, RIG}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, Acvr1b (activin A receptor, type 1B) [NCBI Gene 11479] {aka 6820432J04, ALK-4, ActR-IB, ActRIB, Acvrlk4, Alk4}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, Gdf2 (growth differentiation factor 2) [NCBI Gene 12165] {aka Bmp9}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, Acvr2b (activin receptor IIB) [NCBI Gene 11481] {aka 4930516B21Rik, AI047905, ActRIIB}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, INHBE (inhibin subunit beta E) [NCBI Gene 83729]
- **Diseases:** SO (MESH:D009765), diastolic dysfunction (MESH:D018487), cachexia (MESH:D002100), myocardial (MESH:D009202), Duchenne muscular dystrophy (MESH:D020388), metabolic dysregulation (MESH:D021081), Metabolic abnormalities (MESH:D008659), neuromuscular junction abnormalities (MESH:D020511), skeletal muscle deterioration (MESH:D005207), mitral regurgitation (MESH:D008944), diminished muscle mass and function (MESH:C536030), loss (MESH:D016388), Myocardial fibrosis (MESH:D005355), Hyperglycemia (MESH:D006943), cardiometabolic-musculoskeletal disorders (MESH:D024821), left ventricular dilatation (MESH:C565277), Sarcopenia (MESH:D055948), muscle atrophy (MESH:D009133), Chronic inflammation (MESH:D007249), muscle (MESH:D019042), mitochondrial dysfunction (MESH:D028361), Dyslipidemia (MESH:D050171), diabetic (MESH:D003920), endothelial dysfunction (MESH:D014652), impaired (MESH:D060825), myocardial edema (MESH:D004487), ventricular dysfunction (MESH:D018754), mitral valve prolapse (MESH:D008945), HF (MESH:D006333), adipose tissue dysfunction (MESH:D018205), low muscle strength (MESH:D009800), cardiac (MESH:D006331), cardiac remodeling (MESH:D020257), muscle deterioration (MESH:D009135), chronic (MESH:D002908), systolic and diastolic dysfunction (MESH:D054144), HFrEF (MESH:D054143), microvascular dysfunction (MESH:D017566), amyotrophic lateral sclerosis (MESH:D000690), aortic stiffness (MESH:C566100), LV hypertrophy (MESH:D017379), hypertension (MESH:D006973), impaired quality of life (MESH:D003643), nutritional deficiencies (MESH:D044342), hypertrophy (MESH:D006984), endocrine dysregulation (MESH:D004700), Cardiovascular remodeling (MESH:D002318), Insulin resistance (MESH:D007333), vascular compromise (MESH:D057772), Vascular dysfunction (MESH:D002561)
- **Chemicals:** AGEs (MESH:D017127), resveratrol (MESH:D000077185), vitamin D (MESH:D014807), oxygen (MESH:D010100), salt (MESH:D012492), ATP (MESH:D000255), lipids (MESH:D008055), N-acetylcysteine (MESH:D000111), calcium (MESH:D002118), ROS (MESH:D017382), glucose (MESH:D005947), creatinine (MESH:D003404), 23Na (-), sodium (MESH:D012964), fatty acid (MESH:D005227)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12935647/full.md

## References

75 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935647/full.md

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Source: https://tomesphere.com/paper/PMC12935647