Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo

Michelle Lohbihler, Amos A. Lim, Stéphane Massé, Maggie Kwan, Omar Mourad, Olya Mastikhina, Brandon M. Murareanu, Malak Elbatarny, Renu Sarao, Beiping Qiang, Wahiba Dhahri, Matthew L. Chang, Alice L.Y. Xu, Amine Mazine, Shahryar Khattak, Sara S. Nunes, Kumaraswamy Nanthakumar, Michael A. Laflamme, Stephanie Protze

Posted on: 27 October 2025 , updated on: 29 October 2025

Preprint posted on 4 September 2025

Biological conduction bridges skip a beat. The preprint authors generate AV node-like pacemaker cells from human pluripotent stem cell populations in order to create a biological conduction bridge.

Selected by Theodora Stougiannou

Categories: bioengineering, cell biology

‘Biological conduction bridges (BioCB) skip a beat’

Figure 1. Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo’

Background: The atrioventricular node (AVN) is a structure located between the atrial and ventricular heart chambers, found right beneath the endocardium of the right atrium [1]. It receives electrical impulses originating in the atria, usually from the sinoatrial node (SAN) and then allows for these impulses to be transmitted to the ventricles, coordinating contraction of atrial and ventricular chambers. As the fibrous cardiac skeleton is impervious to electrical transmission, the only route of impulse transmission between atria and ventricles is the AVN which in turn connects to other specialized conduction structures located in interventricular tissue, the bundle of His [1]. This separation between atrial and ventricular myocardium is characteristically observed in crocodiles, birds and mammals.

AV block can be described as the delay in, or complete absence of impulse conduction from atria to ventricles; it can be due to structural or functional impairment in AVN function, caused by e.g. various antiarrhythmic substances, ischemic and degenerative disease, as well as by local manipulation in cardiac surgery (during surgical aortic valve replacement, for example [1]).

AV block is usually tackled via implantation of an electronic pacemaker (EPM). The implantation sites employed for pacemaker insertion can include the right ventricular apex (right ventricular pacing [RVP]), a location often associated with intra-ventricular (within ventricles) and inter-ventricular (between ventricles) dyssynchrony, affecting the function of the heart as a pump [2] [3] [4]. While pacing in the right ventricular septum has been proposed as an alternative, as with apex pacing, it can also lead to cardiomyopathy, particularly when ventricular pacing burden exceeds 50% [5]. Pacing in the bundle of His (His bundle pacing [HBP]) is considered to follow physiologic principles of electrical activation in the ventricle, and is described as an alternative to both RVP and biventricular pacing [6]. Though it can improve on the dyssynchrony and associated heart failure hospitalizations, it can be associated with electrical disruptions in the form of P-wave oversensing and R-wave undersensing. Another alternative to the transvenous pacemakers for tackling AV block is leadless pacing (LL), where single- or multicomponent devices are implanted in the myocardium. In the case of multicomponent devices, proper wireless communication between these is required, while battery longevity as well as additional issues around the implantation procedure have also been identified[7]. In short, there is a need to develop biological Conduction Bridges (BioCB) with more favorable biological profiles compared to current implanted pacemaker devices.

During embryonic development cardiac progenitors originate from mesodermal progenitor groups; differentiation protocols thus make use of the signaling required during these stages to generate specific cardiac progenitor groups and cardiac cells in vitro. Ventricular-like cardiomyocytes (VLCM) can be generated with cardiac induction media containing the Wnt signaling inhibitor IWP2 along with VEGF. Atrial-like cardiomyocytes (ALCM) can be generated with cardiac induction media containing IWP2, VEGF along with RA. Sinoatrial-like pacemaker cells (SANLPC) are generated from RALDH2+ mesoderm with WNT inhibition followed by RA, BMP signaling and FGF signaling inhibition. The study by Lohbihler and team seeks to generate AV node-like pacemaker cells from human Pluripotent stem cell (PSC) populations using appropriate signaling modulation. These AVN-like pacemaker cells (AVNLPC) are generated with supplementation of BMP2 after culturing in cardiac induction media used for VLCM derivation [4] [8].

Key aspects of the study:

AVNLPC can be identified by their expression of TBX3, NKX2-5:
1. Activation of WNT signaling via CHIR99021 administered between days 8-11 led to generation of CHIR99021-derived AVNLPC (first detected on day 6).
2. Activation of BMP signaling via BMP2 administered between days 5-8 led to the generation of BMP2-derived AVNLPC (first detected on day 6).
BMP2-derived AVNLPC resemble fetal core AVN pacemaker cells:
1. BMP2-derived AVNLPC were evaluated via RNA-sequencing (RNA-seq) (day 20) with GO analysis of biological processes enriched in the TNNT2+ cardiomyocyte cluster linking to processes of regulation of heart contraction, cardiac conduction, cardiac pacemaker differentiation, AV node cell action potential, AVN cell differentiation [4].
2. Comparison to RNA-sequencing data of human fetal AVN tissue confirmed that AVNLPCs resemble fetal AVN pacemaker cells.
AVNLPC generated from the ESI-017-ASAP1 cell line exhibit electrophysiological properties comparable to the AVN in vitro:
1. Engineered AVN tissues (eAVNT) exhibited higher rates of diastolic depolarization, slower maximum upstroke potential velocities compered to engineered ventricular tissue; no difference in action potential duration at 30% and 90% of repolarization was observed [4].
2. Pacing from the bottom with 2.5Hz led to slow conduction velocities in the eAVNT (3.8±1.5 cm/s) compared to eVT (12.8±2.8cm/s); these slower conduction velocities observed in the eAVNT were comparable to those observed physiologically in humans [4].
3. Simulation of fast atrial rhythms by increasing the pacing frequency showed a 1:1 impulse capture ratio by eAVNT until the limit of 3.3±0.2 Hz was reached, a physiological equivalent of 198 beats/min; upon further increase of the pacing frequency, the eAVNT exhibited a conduction block of 2:1 ultimately reaching a ratio of 4:1. No such conduction delay was observed in the eVT engineered tissue, which showed a 1:1 capture ratio up until 4.8±0.3 Hz, a physiological equivalent of 288 beats/min [4].
4. eAVNT also exhibited decremental conduction, similar to the endogenous AVN.
When transplanted into animal models in vivo, AVNLPC exhibit electrophysiological properties comparable to the AVN:
1. A guinea pig cryoinjury model was used to create scar tissue and thus, an electrical conduction block in the left ventricular free wall. AVNLPC generated from the ESI-017-ASAP1 or VLCM were then injected into the border zone of the resulting ventricular myocardial scar and hearts were studied 2 to 4 weeks after the injection [4].
2. Heart pacing at 2Hz showed synchronization and electrical coupling between AVNLPC or VLCM grafts (ASAP1) and guinea pig hearts (RH237)[4].
3. Cessation of heart pacing showed sustained ventricular ectopic beats in all tested animals with AVNLPC grafts, indicating electrical pacing originating from the graft; only 2 out of 7 animals with VLCM exhibited sustained ectopic pacing and the remaining 5 out of 7 animals showed only some sporadic ectopic beats [4].
4. AVNLPC grafts exhibited the pacemaker phenotype seen in in vitro experiments, with diastolic depolarization and slower maximum upstroke velocity, when compared with VLCM grafts [4].
AVNLPC grafts block the conduction of rapid rhythms when transplanted into animal models in vivo:
1. Upon heart pacing at 2Hz, AVNLPC grafts displayed conduction in the range of physiological human conduction observed by the AVN, at 13.5±7.4 cm/s; conversely, conduction velocities observed in the VLCM grafts were much higher, at 34.5±14.7 cm/s [4].
2. Upon heart pacing at increasing frequencies, AVNLPC grafts showed a 1:1 electrical impulse capture ratio, until the 3.0±0.7 Hz was reached; conversely, VLCM grafts exhibited a 1:1 electrical impulse capture ratio until a higher limit is reached at 6.6±1.4Hz. This highlights the ability of the AVNLPC graft in this study to successfully prevent the transmission of fast atrial rates [4].
Grafts maintain their molecular identity throughout the entire engraftment period, as shown by the cTNT+ MSX2+ staining observed in AVNLPC grafts and the cTNT+ MSX2^low staining observed in VLCM grafts[4].

Why this work is interesting:

The study by Lohbihler and colleagues, carries out a comprehensive evaluation of AVNLPC populations both in vitro and in vivo using a guinea pig model. These cell populations were derived from embryoid bodies (EB) and not adherent monolayer cultures, allowing for the adaptation of these protocols to bioreactor-based protocols and future large scale production [4]. The study also demonstrates the presence of NKX2-5+TBX3+ cardiomyocytes, corresponding to pacemaker cells, derived via standard ventricular cardiomyocyte protocols which can negatively affect cell therapy aimed at treating myocardial infarction. Removal of pacemaker cells by inhibiting BMP signaling after cardiac progenitors are specified can further purify populations meant for myocardial cell therapy, enhancing therapeutic safety [4].

The AVNLPCs derived in this protocol can be used to derive a so-called biological conduction bridge (BioCB) and can be engrafted into the corresponding locations within mammalian hearts to restore conduction in vivo. In the animal model in this study, cells were engrafted via thoracotomy directly onto the injured myocardium (while immunosuppression was also applied to prevent graft rejection) [4]. The engraftment procedure will be easier in larger models, fully ensuring an engraftment area spanning from atria to ventricles; in addition, ensuring these grafts maintain their molecular profile and safe function within human physiological limits is crucial, something which is indeed observed in this study. However, since the AVN is a heterogenous biological structure, the authors acknowledge that further studies evaluating the signaling pathways driving differentiation of each of the cardiomyocyte subtypes identified in the AVN can help generate engineered tissue more closely resembling native AVN structures [4].

Authors one sentence statement on impact of the study:

“This is the first study generating human pluripotent stem-cell derived AVN-like pacemaker cells and demonstrating their functionality for biological conduction bridge applications in vivo”.

Glossary of interesting terms used in this preLight:

Sinoatrial node (SAN): Characterised as the dominant pacemaker in the heart, found between the superior vena cava and the right atrium [9].
Atrioventricular node (AVN): Conducts electrical impulses from the atria to the ventricles, an interatrial structure located beneath the endocardium of the right ventricle [1].
Ventricular conduction system (VCS): Comprises the bundle of His, the left and right bundle branches and lastly, the Purkinje fibers; coordinates contraction of the right and left ventricles with the atria [9].
Atrioventricular canal (AVC): Transient structure appearing during development, separating developing atria and ventricular tissue.
Pluripotent stem cells (PSC): Stem cells with the capability to differentiate towards all 3 germ layers of the developing embryo (endoderm, mesoderm, ectoderm) as well as extraembryonic tissues (hypoblast, extraembryonic or primitive endoderm, extraembryonic mesoderm)
CHIR99021: Small molecule used to induce the WNT signaling pathway; inhibits Glycogen synthase kinase β (GSKβ), thus preventing the phosphorylation and degradation of β-catenin by GSKβ.
Inhibitor WNT production-2 (IWP2): Small molecule used to inhibit WNT signaling, often used to induce cardiac mesoderm from mesoderm progenitors.
ASAP1: Fluorescent voltage sensor protein based on a voltage-sensitive phosphatase protein; in this protein the phosphatase domain is removed and a GFP is added in the S3-S4 linker of the molecule. It is used to visually track action potentials, as it gives off green fluorescence in response to changes in action potential. In this study, ASAP1 is used to track electrical activity in the cellular grafts.
RH237: Voltage-sensitive dye, used to track action potentials in cells such as cardiomyocytes; in this study, RH237 is used to track voltage changes in host guinea pig hearts.

References:

[1] Issa ZF, Miller JM, Zipes DP. Chapter 9 – Atrioventricular Conduction Abnormalities. In: Issa ZF, Miller JM, Zipes DP, editors. Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald’s Heart Disease (Second Edition), Philadelphia: W.B. Saunders; 2012, p. 175–93. https://doi.org/10.1016/B978-1-4557-1274-8.00009-9.

[2] Mashali MA, Saad NS, Peczkowski KK, Fanning T, Hare AN, Whitson BA, et al. Mechanical Dyssynchrony of Isolated Left and Right Ventricular Human Myocardium in End-Stage Heart Failure. Circulation: Heart Failure 2023;16:e009871. https://doi.org/10.1161/CIRCHEARTFAILURE.122.009871.

[3] Tops LF, Schalij MJ, Holman ER, van Erven L, van der Wall EE, Bax JJ. Right Ventricular Pacing Can Induce Ventricular Dyssynchrony in Patients With Atrial Fibrillation After Atrioventricular Node Ablation. Journal of the American College of Cardiology 2006;48:1642–8. https://doi.org/10.1016/j.jacc.2006.05.072.

[4] Lohbihler M, Lim AA, Massé S, Kwan M, Mourad O, Mastikhina O, et al. Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo 2025:2025.09.04.674322. https://doi.org/10.1101/2025.09.04.674322.

[5] Biffi M, Bagatin A, Spadotto A, Lazzeri M, Carecci A, Bartoli L, et al. Atrioventricular Block Treatment: Pacing Site, AV Synchrony, or Both? Journal of Clinical Medicine 2025;14:980. https://doi.org/10.3390/jcm14030980.

[6] Lewis AJM, Foley P, Whinnett Z, Keene D, Chandrasekaran B. His Bundle Pacing: A New Strategy for Physiological Ventricular Activation. Journal of the American Heart Association 2019;8:e010972. https://doi.org/10.1161/JAHA.118.010972.

[7] Lee JZ, Mulpuru SK, Shen WK. Leadless pacemaker: Performance and complications. Trends in Cardiovascular Medicine 2018;28:130–41. https://doi.org/10.1016/j.tcm.2017.08.001.

[8] Kim M-S, Horst A, Blinka S, Stamm K, Mahnke D, Schuman J, et al. Activin-A and Bmp4 Levels Modulate Cell Type Specification during CHIR-Induced Cardiomyogenesis. PLOS ONE 2015;10:e0118670. https://doi.org/10.1371/journal.pone.0118670.

[9] Park DS, Fishman GI. 29 – Cell Biology of the Specialized Cardiac Conduction System. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology: From Cell to Bedside (Sixth Edition), Philadelphia: W.B. Saunders; 2014, p. 287–96. https://doi.org/10.1016/B978-1-4557-2856-5.00029-7.

doi: https://doi.org/10.1242/prelights.41818

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Author's response

Stephanie Protze, Michelle Lohbihler shared

Would complete cellular and histological replication of the native AVN further enhance the functionality of biological conduction bridges such as the one presented in this work, or is it better to keep their structure simpler to better control their biological function in vivo?

“Replicating the full cellular and histological complexity of the native AVN could enhance the functionality of a biological conduction bridge, as proper conduction depends on the integration and coordination of several cellular subtypes with a gradient of electrophysiological properties. The AVN is not a homogeneous structure but consists of the atrial transition zone (ATZ), compact or core AVN, and the lower nodal bundle (LNB), each contributing uniquely to impulse delay and propagation. Therefore, recreating this continuum of specialized cell types and spatial organization might be ideal for achieving physiological conduction and proper signal propagation”.

“That said, increasing biological complexity may also cause more challenges. More heterogeneous tissues can introduce variability and make in vivo transplantation harder to control. Beyond that, including additional cell types will make the barrier for approval from regulatory agencies much higher. A logical next step would therefore be to begin with a simpler version of a biological conduction bridge (BioCB) including only AVNLPCs to confirm their ability to safely re-establish slow conduction in a large-animal model”.

What is next after this study? Do you believe it’s better to carry out similar experiments in small animal models, with the added difficulty of correctly positioning the biological conductor to span the area between atria and ventricles, or would the use of larger animal models be applicable at this stage?

“The anatomical and surgical constraints of small animal models like the guinea pig limit how well we can inject AVNLPCs spanning from the right atrial chamber to the ventricles to create a biological conduction bridge (BioCB). Larger animal models with improved surgical accessibility will be necessary to evaluate AVNLPCs’ potential to re-establish conduction between the atria and ventricles and treat AV-block. The ideal model would be the pig, which is widely regarded as the gold standard pre-clinical animal model in cardiac research. A logical next step would therefore be to create a complete AV-block model in pigs via AVN ablation and to assess the safety and function of an AVNLPC-based BioCB”.

As I am involved in clinical cardiovascular research, we oftentimes see patients with sequelae from their implanted pacemakers, that often require surgical repositioning of the pacemaker battery. It would be interesting to learn more about the timeline that you would propose for such biological implants to reach clinical translation?

“It’s still very early and there are a lot of unknowns that will need to be determined in large-animal studies before moving to human clinical trials. Large-animal studies will be critical to evaluate integration with the other components of the cardiac conduction system, long-term stability and safety. It will be important to ensure that the conduction properties of the BioCB remain consistent over time without functional deterioration. Long-term monitoring will also be necessary to assess potential risks, including the emergence of re-entry circuits or ectopic pacemaker activity, both of which could lead to arrhythmias. Additionally, the ability of the BioCB to respond appropriately to autonomic inputs – such as during exercise or stress – will need to be determined. Beyond that, the best surgical approach for cell delivery must be determined, with a preference for minimally invasive techniques. Therefore, transcatheter injection methods should be explored to avoid open-heart surgery. So, realistically, clinical translation might still be a decade or more away. Our current study demonstrates the potential of AVNLPCs and marks an exciting first step towards a future BioCB”.

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Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo

‘Biological conduction bridges (BioCB) skip a beat’

Figure 1. Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo’

Authors one sentence statement on impact of the study:

“This is the first study generating human pluripotent stem-cell derived AVN-like pacemaker cells and demonstrating their functionality for biological conduction bridge applications in vivo”.

References:

[2] Mashali MA, Saad NS, Peczkowski KK, Fanning T, Hare AN, Whitson BA, et al. Mechanical Dyssynchrony of Isolated Left and Right Ventricular Human Myocardium in End-Stage Heart Failure. Circulation: Heart Failure 2023;16:e009871. https://doi.org/10.1161/CIRCHEARTFAILURE.122.009871.

[4] Lohbihler M, Lim AA, Massé S, Kwan M, Mourad O, Mastikhina O, et al. Human pluripotent stem cell-derived atrioventricular node-like pacemaker cells exhibit biological conduction bridge properties in vitro and in vivo 2025:2025.09.04.674322. https://doi.org/10.1101/2025.09.04.674322.

[5] Biffi M, Bagatin A, Spadotto A, Lazzeri M, Carecci A, Bartoli L, et al. Atrioventricular Block Treatment: Pacing Site, AV Synchrony, or Both? Journal of Clinical Medicine 2025;14:980. https://doi.org/10.3390/jcm14030980.

[6] Lewis AJM, Foley P, Whinnett Z, Keene D, Chandrasekaran B. His Bundle Pacing: A New Strategy for Physiological Ventricular Activation. Journal of the American Heart Association 2019;8:e010972. https://doi.org/10.1161/JAHA.118.010972.

[7] Lee JZ, Mulpuru SK, Shen WK. Leadless pacemaker: Performance and complications. Trends in Cardiovascular Medicine 2018;28:130–41. https://doi.org/10.1016/j.tcm.2017.08.001.

[8] Kim M-S, Horst A, Blinka S, Stamm K, Mahnke D, Schuman J, et al. Activin-A and Bmp4 Levels Modulate Cell Type Specification during CHIR-Induced Cardiomyogenesis. PLOS ONE 2015;10:e0118670. https://doi.org/10.1371/journal.pone.0118670.

[9] Park DS, Fishman GI. 29 – Cell Biology of the Specialized Cardiac Conduction System. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology: From Cell to Bedside (Sixth Edition), Philadelphia: W.B. Saunders; 2014, p. 287–96. https://doi.org/10.1016/B978-1-4557-2856-5.00029-7.

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