Regarding the cellular and molecular events in wound healing, all of the following statements are correct EXCEPT:

Explanation

## Wound Healing Phases and Cellular Events ### Overview of Wound Healing Phases Wound healing occurs in three overlapping phases: **inflammatory** (0–3 days), **proliferative** (3–21 days), and **remodeling** (weeks to years). Each phase involves distinct cellular and molecular players. ### Analysis of Each Statement | Statement | Accuracy | Explanation | |-----------|----------|-------------| | Myofibroblasts and wound contraction | **Correct** | Myofibroblasts are activated fibroblasts expressing α-smooth muscle actin (α-SMA). They generate contractile forces via actin–myosin interactions, reducing wound area by 10–20% during remodeling. | | TGF-β as primary inflammatory cytokine | **INCORRECT** | TGF-β is secreted by **multiple cell types** (macrophages, platelets, T cells, fibroblasts, endothelial cells), not exclusively by neutrophils. It is also a key **proliferative** and **remodeling** phase cytokine, not just inflammatory. | | VEGF-mediated angiogenesis | **Correct** | VEGF is the master regulator of angiogenesis. It promotes endothelial cell proliferation, migration, and tube formation, essential for restoring blood supply to healing tissue. | | Proliferative phase timing and features | **Correct** | The proliferative phase begins ~day 3–4, peaks at day 5–7, and is hallmarked by fibroblast proliferation, type I and III collagen deposition, and granulation tissue formation. | ### Key Point: **TGF-β is NOT secreted exclusively by neutrophils.** It is produced by macrophages (the dominant source during inflammation), platelets, T cells, fibroblasts, and endothelial cells. Additionally, TGF-β is a **multiphase cytokine** — it initiates inflammation but is also critical in proliferation and remodeling. ### High-Yield: Common NEET PG trap: conflating the **source** of cytokines. Neutrophils produce IL-1, TNF-α, and proteases; macrophages produce TNF-α, IL-1, IL-6, **TGF-β**, and VEGF. Know the primary sources. ### Clinical Pearl: In chronic wounds (e.g., diabetic ulcers), excessive TGF-β signaling can lead to pathologic fibrosis, while insufficient VEGF results in poor angiogenesis and impaired healing.