CLAD: translating basic science to clinical practice
Evidence level: review-abstract-only
A narrative review in the Journal of Heart and Lung Transplantation, published online 9 October 2026, that proposes classifying CLAD by biological endotypes. Only the abstract was read.
As of . Primary source: Burman et al. 2026, J Heart Lung Transplant (DOI; abstract only was read).
Summary
Narrative review, not a new study. The abstract describes CLAD as the fibrotic manifestation of chronic rejection and a major barrier to long-term survival. It describes CLAD as the final common pathway of diverse alloimmune injuries, augmented by non-alloimmune insults. It names cytotoxic and senescent T cells, humoral immunity, innate immune activation, epithelial dysfunction, aspiration and dysbiosis. It proposes a shift from the clinical phenotypes BOS and RAS toward biologically defined endotypes that may better predict progression and therapeutic response. It recognises ALAD as a heterogeneous syndrome that offers a chance to characterise graft injury before irreversible fibrosis. The biomarkers named, which are donor-derived cell-free DNA, airway transcriptomic signatures, autoantibodies, epithelial injury markers and microbiome-derived signals, may aid risk stratification, patient enrichment and endotype-guided trials. Only the abstract of the source review was read; the full text was not read.
Details
- doi
- 10.1016/j.healun.2026.10.005
- pmid
- 42854767
- authors
- Burman A (Toronto Lung Transplant Program, University Health Network); Bell PT (Queensland Lung Transplant Service, The Prince Charles Hospital, Brisbane, and University of Queensland); Chambers D (Queensland Lung Transplant Service, The Prince Charles Hospital, Brisbane, and University of Queensland); Martinu T (Toronto Lung Transplant Program, University Health Network, and University of Toronto; corresponding author)
- journal
- Journal of Heart and Lung Transplantation
- year
- 2026
- publishedOnline
- 2026-10-09
- articleType
- narrative review
Sources and links
Related
Links from this record
- author (last author, corresponding): Tereza Martinu
- affiliation: Toronto Lung Transplant Program (University Health Network)
- discusses: Bronchiolitis obliterans syndrome (BOS)
- discusses: Restrictive allograft syndrome (RAS)
- proposes: Molecular endotypes of CLAD (proposed framework)
- discusses: Acute lung allograft dysfunction (ALAD)
Linked from (derived)
- described in (abstract only): Acute lung allograft dysfunction (ALAD)
- proposed in (abstract only): Molecular endotypes of CLAD (proposed framework)
- described in (abstract only): Airway epithelial dysfunction
- described in (abstract only): Aspiration
- described in (abstract only): Cytotoxic and senescent T cells
- described in (abstract only): Humoral (antibody-mediated) alloimmunity
- described in (abstract only): Innate immune activation
- described in (abstract only): Microbial dysbiosis
- named in (abstract only): Airway transcriptomic signatures
- named in (abstract only): Autoantibodies
- named in (abstract only): Donor-derived cell-free DNA
- named in (abstract only): Epithelial injury markers
- named in (abstract only): Microbiome-derived signals
- evidence: No validated molecular endotype scheme exists for CLAD
Known gaps in this record
- full text of the source review not read, so the evidence, citations and level of agreement for this item are missing
- funding and conflicts of interest of the source review not read
- affiliations of the authors are taken from the record as described in the briefing and were not independently re-checked
Information resource only. Not medical advice. Not a substitute for the care of the patient's transplant team.