Vincent Kawuribi, Peipei Dou, Xiaomei Deng, Wenjun Wang, Heyun Tang, Shaohui Zheng, Qiang Wang
Microbiological cure of tuberculosis (TB) does not restore normal lung health. Roughly half of TB survivors develop post-tuberculosis lung disease (PTLD), characterized by fibrosis, cavitation, bronchiectasis, and chronic inflammation, and lung cancers frequently arise in or near residual TB scars. This oncogenic risk is under-recognized, and post-TB surveillance remains largely passive, relying on static imaging and low-sensitivity biomarkers that perform poorly in structurally complex lungs. We argue that the central limitation of current surveillance is a mismatch between a dynamic, spatially heterogeneous pathology and inherently static diagnostic tools. Synthesizing clinical and mechanistic evidence, we describe how the post-TB lung is reshaped along three converging axes, namely structural remodeling, immune dysfunction, and metabolic stress, that together recapitulate features of the tumor microenvironment. We then examine nanomotors, a class of self-propelled diagnostic agents able to navigate complex biological media, overcome diffusion and sampling limits, and functionally map high-risk niches. Prioritizing translational feasibility, we focus on near-term applications such as ex vivo biomarker enrichment in sputum and bronchoalveolar lavage fluid, and we place more speculative sensing and therapeutic uses on a staged roadmap. This framework reframes the post-TB lung as an active scar and outlines a biologically aligned strategy for earlier cancer detection and risk-modifying intervention in TB survivors.